ProgramandAbstracts - eksideksid.com/pds/files/20______________________.pdf · ProgramandAbstracts 2010.4.2 ... Jeong-Hyun Shin2, SunA Yoon 3, Sang-Joo Park3, ... Tae Kyun Kim, Jin

The 20th Academic Meeting of KoreanSociety for Investigative Dermatology

Program and Abstracts

2010. 4. 2(FRI)~3(SAT)

Auditorium, 1st Floor, Clinical Research InstituteSeoul National University Hospital, Seoul, Korea

Hosted by Korean Society for Investigative Dermatology (KSID)

Sponsored by Korean Dermatological Association (KDA)

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Greetings

Greeting to the KSID members,

The year 2010 was begun andwe all hope our KSIDmembers and researchers

interested in skin biology start this year with hope and prosperity.

On behalf of the KSIDmembers, we would like to send our deep appreciation

to all the KSIDmembers and people who have been support us for their endless

endeavor and co-operation to prosper the basic science in dermatology.

And we also notify the 20th KSID annual meeting at April 2~3, 2010.

In the 20th KSID annualmeeting as the same in the previous annualmeetings,

we have a plan to make progress with academic conference, symposium and

skin biology research training programs.

The main subjects of this year’s symposium are Epithelial and Mesenchymal

cell Transition (EMT) and recent progress in skin biology related scientific field,

and the main theme in the training programs are recent progress in skin cell

research and in extracellular matrix. We already invite 4 worldwide famous

doctors-Professor Kang Sewon (Johns Hopkins University, USA), Professor

Shigetoshi Sano (Kochi University, Japan), Professor Hironobu Ihn (Kumamoto

University, Japan) and Professor Chun-Di He (China Medical University,

China) and we prepare the lots of lectures and presentations from eminent

professors and researchers Korean nationwide and also from JSID.

We all wish you to attend the 20th KSID meeting and to glorify the name of

KSID in spite of your busy works and/or researches.

2010 March

Korean Society for Investigative Dermatology

Chairman of Board Jun Mo YangPresident Kee Chan Moon

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Symposium (I) EMT (Epithelial and Mesenchymal Cell Transition)

Symposium (II) Recent Progress in Skin Research

Program

2 April, 2010 (Fri)

08:30-09:00 Registration

Chairs : Dongsik Bang, Kwang Hyun Cho

09:00-09:30 EMT-Overview and basic theory / 18

Woo Ho Kim (Soul National Univ, Korea)

09:30-10:00 EMT & wound healing / 21

Duk Hee Kang (Ewha Womans Univ, Korea)

10:00-10:30 Differentiation-related expression of class II beta-tubulin in skin / 23

Sun Ho Kee (Korea Univ, Korea)

10:30-11:00 Coffee Break

11:00-11:50 Invited Lecture I: Sponsored by Leaders Skin Clinic

Chair : Kee Chan Moon

Recent progress in psoriasis research on mechanistic interaction / 28

between cytokines and keratinocytes: a distinct role of the IL-23/ Th17 axis

Shigetoshi Sano (Kochi Univ, Japan)

11:50-12:40 Invited Lecture II: Sponsored by Clean Up Skin Clinic

Chair : Jai Il Youn

Hair lost in translation: what can we learn from the recent / 30

study about Marie Unna hereditary hypotrichosis (MUHH)

Chun-Di HE (China Medical Univ, China)

12:40-13:50 Photo & Lunch

13:50-14:00 Opening Ceremony

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14:00-15:00 Plenary Lecture (I) Chair : Hee Chul Eun

Improving photoaged skin with lasers, dermabrasion and topical / 41

5-FU: in search of an unifying principle

Sewon Kang (Johns Hopkins Univ, USA)

15:00-16:00 Free Communication (I) Chairs : Kyu Suk Lee, Tae Yoon Kim

FC-1 Early-onset sarcoidosis and Blau syndrome: autoinflammatory granulomatosis / 55

associated with NOD2 mutations causing constitutive NF-kappaB activation

Nobuo Kanazawa

Department of Dermatology, Wakayama Medical University, Wakayama, Japan

FC-2 HMG-CoA reductase inhibitors have an inhibitory effect on Th17 cytokines- / 56

induced CCL20 expression in keratinocytes in vitro

Taegyun Kim, M.D.2, Dashlkhumbe Byamba, M.D.2, Jung Hwan Je, Ph.D.1,

Jin Mo Park, M.D.1, Hyo Jin Roh, M.D.1, Min-Geol Lee, M.D., Ph.D.1

1Department of Dermatology and Cutaneous Biology Research Institute, Brain Korea 21 Project for Medical

Science, Yonsei University College of Medicine, Seoul, Korea; 2These Authors Equally Contributed to this Work

FC-3 Callus is formed by hyperproliferation with incomplete differentiation and / 57

increase of adhesive molecules in the epidermis

Su Hee Kim1, Soo Il Kim1, Hye In Choi1, Young Jin Choi1, Kyung Cheol Sohn2,

Young Lee2, Chang Deok Kim2, Jeung Hoon Lee2, Young Ho Lee1

Departments of 1Anatomy, 2Dermatology, School of Medicine, Chungnam National University

FC-4 Expression and functional role of Sox9 in keratinocyte differentiation / 58Ge Shi1, Zheng jun Li1, Kyung-Cheol Sohn1, Dae-Kyoung Choi1, Young Ho Lee2,

Tae-Jin Yoon3, Young Lee1, Chang Deok Kim1, Jeung-Hoon Lee1

1Departments of Dermatology, 2Anatomy,School of Medicine, Chungnam National University, Daejeon;3Department of Dermatology, School of Medicine, Gyeongsang National University, Jinju, Korea

16:00-17:00 Free Communication (II) Chairs : Hae Jun Song, Min Geol Lee

FC-5 H19 RNA downregulation stimulated melanogenesis in melasma / 59

Yun-Seok Choi1, Nan-Hyung Kim

1, Chang-Hoon Lee

2, Ai-Young Lee

1

1Department of Dermatology, Dongguk University School of Medicine, 2Division of Basic Science,

National Cancer Center, Goyang, Korea

FC-6 Identification of up-regualted proteins in psoriasis vulgaris using proteomics / 60Jae-We Cho, Kyu-Suk Lee

Department of Dermatology, School of Medicine, Keimyung University

FC-7 MyD88 mediates UV-induced inflammatory responses and cell apoptosis / 61

in mouse skin in vivoYoungae Lee, Kyung-hwan Kong, Se Rah Lee, Hyun-Sun Yoon, Kyu Han Kim, Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine; Laboratory of Cutaneous Aging

Research, Clinical Research Institute, Seoul National University Hospital; Institute of Dermatological Science,

Seoul National University, Seoul, Korea.

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FC-8 -catenin regulates melanocyte dendricity through the modulation ofβ / 62PKC and PKCζ δ

Jin-Hwa Kim1, Kyung-Cheol Sohn2, Tae-Young Choi2, Mi Yoon Kim2, Hideya Ando3,4,

Sun Ja Choi5,6, Sooil Kim7, Young Ho Lee7, Jeung-Hoon Lee2, Chang Deok Kim2, Tae-Jin Yoon1

1Department of Dermatology and Institute of Health Sciences, School of Medicine, Gyeongsang National

University, Jinju; 2Department of Dermatology and Research Institute for Medical Sciences, School of Medicine,

Chungnam National University, Daejeon, Korea. 3Skin Aging and Photo-aging Research Center, Doshisha

University, Kizugawa, Kyoto; 4Kobe Skin Research Institute, Kobe, Hyogo, Japan. 5Department of Visual

Design, Daeduk University, Daejeon;. 6Department of Advanced Organic Materials Engineering, Chonbuk

National University, Jeonju; 7Department of Anatomy, School of Medicine, Chungnam National University,

Daejeon, Korea.

17:00-17:30 Invited Lecture III: Sponsored by Kye Skin Clinic Chair : Kwang-Hoon Lee

Molecular mechanism of fibrosis / 32

Hironobu Ihn (Kumamoto Univ, Japan)

18:00- Welcome Reception

3 April, 2010 (Sat)

09:00-09:30 UAM Award Lecture Chair : Young Ho Won

The Increased Expression of Matrix Metalloproteinase-9 Messenger / 34

RNA in the Non-lesional Skin of Patients with Large Plaque Psoriasis Vulgaris

Wook Lew (Yonsei University College of Medicine, Seoul, Korea)

09:30-10:20 Plenary Lecture (II) Chair : Jeung Hoon Lee

Harnessing ultraviolet light to improve skin fibrosis / 42

Sewon Kang (Johns Hopkins Univ, USA)


10:40-11:30 Hot Posters Chairs : Kyu Joong Ahn, Kyu Han Kim

11:30-12:00 Research in Industry Chair : Chang Kwun Hong

Insight Mining Through Meta-Analysis of Public Microarray Databases / 46

Minsoo Noh (Amore-Pacific Co. Ltd., Korea)

12:00-12:30 Bench to Clinic Chair : Do Won Kim

From Bench to Bedside in the Application of Stem Cells / 51

Byung Soon Park (Leaders Clinic, Korea)

12:30-14:00 Lunch & Business Meeting

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Training Course in Cutaneous Biology

14:00-15:30 Recent progress in skin cell research

Chairs : Soo Chan Kim, Mu Hyung Lee

1. Keratinocyte / 67

Jeung Hoon Lee (Chungnam National Univ, Korea)

2. Recent knowledge in melanocyte research / 69

Hee Young Kang (Ajou Univ, Korea)

3. Langerhans cell and dermal dendritic cell / 73

Min-Geol Lee (Yonsei Uinv, Korea)


15:50-17:20 Recent rogress in ECM Chairs : Jee Ho Choi, Tae Jin Yoon

4. ECM production by fibroblasts / 76

Jin Ho Chung (Soul National Univ, Korea)

5. Cross-talk between ECM and TGF-beta signaling / 79

Suntaek Hong (Gachou Univ, Korea)

6. Collagen, elastin, reticular fiber / 81

Kee Yang Chung (Yonsei Univ, Korea)

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Oral Poster

PO-1 Activators of Peroxisome Proliferator-Activated Receptor alpha (PPAR )α / 85

protect UV-induced changes of MMP-1 and procollagen via catalase

induction in human skin fibroblasts

Mi Hee Shin, Hyun-Sun Yoon, Dong Hun Lee, Jang-Hee Oh, Eunyoung Seo, Jin Ho Chung

Department of Dermatology, Seoul National University College of Medicine; Laboratory of Cutaneous

Aging Research, Clinical Research Institute, Seoul National University Hospital, and Institute of

Dermatological Science, Medical Research Center, Seoul National University, Seoul, Korea

PO-2 The study of regulatory mechanism of IL-17 induced Egr-1 expression / 86

in HaCaT human keratinocytes

Jae Eun Choi1,2, Sang Hoon Jeong1, Yoon-Hee Park1, Sang Min Lee2, Jae Hwan Kim2,

Il Hwan Kim2, Sang Wook Son1,2, Young Chul Kye1,2

1Laboratory of Cell Signaling and Nanomedicine, 2Department of Dermatology and Division of Brain

Korea 21 Project for Biomedical Science, Korea University College of Medicine, Seoul, Korea

PO-3 Filaggrin knockdown enhanced the production of IL-6, IL-8, and thymic / 87

stromal lymphopoietin from HaCaT cells via TLR stimulation

Kyung Ho Lee1, Kyung-Ah Cho2, Ji-Yoon Kim2, Ji Hye Baek1, So-Youn Woo2, Jin-Woo Kim1

1Department of Dermatology, College of Medicine, The Catholic University of Korea,2Departments of Microbiology, School of Medicine, Ewha Womans University, Seoul, Korea

PO-4 HnRNP-A2/ B1 as a target antigen of anti-endothelial cell IgA / 88

antibody in Behçet’s disease

Sung Bin Cho, M.D., Keun Jae Ahn, Ph.D., Suhyun Cho, M.D., Shin-Wook Kang, M.D.,

Ph.D., Ju Hee Lee, M.D., Ph.D., Yong-Beom Park, M.D., Ph.D., Kwang Hoon Lee, M.D.,

Ph.D., Dongsik Bang, M.D., Ph.D.

Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of

Medicine, Seoul, Korea (S.B.C., K.J.A., S.H.C., J.H.L., K.H.L., D.B.), Division of Nephrology, Department

of Internal Medicine, BK21 Project for Medical Science, Yonsei University College of Medicine, Seoul,

Korea (S-.W.K.). Division of Rheumatology, Department of Internal Medicine, Institute for Immunology

and Immunologic Diseases, BK21 Project for Medical Science, Yonsei University College of Medicine,

Seoul, Korea (Y-.B.P.)

PO-5 Cyclosporine stimulates the expression of CDK4 through NFATc1 / 89

suppression: A good candidate for therapeutic modality in alopecia areata

Chae-Young Lee, Young-Hun Kim, Ki-Ho Kim

Department of Dermatology, Dong-A University College of Medicine

PO-6 A decline of TRPV6 function derives from a decrease of vitamin D / 90

activation and accounts for disturbed epidermal calcium gradient followed

by skin barrier alteration in aged skin

Minyoung Jung1, Yoonhee Lee1, Byung-Il Yeh2, Seung Hun Lee3, Eung Ho Choi1

1Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju;2Department of Biochemistry, Yonsei University Wonju College of Medicine, Wonju;3Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea

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Poster presentations

P-1 Modification of transcription factors with O-linked N-acetylglucosamine / 93

during the process of keratinocyte differentiation

Eun jin Lee, Kyung-Cheol Sohn, Sang-Shin Lee, Jeung-Hoon Lee

Department of Dermatology, School of Medicine, Chungnam National University

P-2 EC-SOD transgenic mice show thin epidermis by apoptosis through / 94

galectin- 7 and COX-2 expression

Joon-seok Lee, Yunsang Lee, and Tae-Yoon Kim

Laboratory of Dermato-Immunology, Catholic Research Institute of Medical Science, College of Medicine,

The Catholic University of Korea

P-3 Assessment of phototoxicity and skin irritation potential of / 95

nanopolystyrene and nanoTiO2 using cultured keratinocytes,

a human skin equivalent model and an in vivo model

Yoon-Hee Park2, Sang Hoon Jeong2, Sang Min Yi1, Jae Hwan Kim1, Jae Eun Choi1,

Byeong Hyeok Choi2, Meyoung-Kon Kim3, Il-Hwan Kim1, Sang Wook Son1

1Department of Dermatology and Division of Brain Korea 21 Project for Biomedical Science, Korea

University College of Medicine, Seoul; 2Laboratory of Cell Signaling and Nanomedicine, Korea University

College of Medicine, Seoul; 3Department of Biochemistry & Molecular Biology, Korea University College

of Medicine, Seoul, Korea

P-4 Our new devised method determining the intial dose of narrow-band / 96

UVB treatment with colorimetric L* value

Jai Il Youn, In Ho Kwon, Hyuck Hoon Kwon

Department of Dermatology, Seoul National University College of Medicine

P-5 Effect of light emitting diodes (LED) on melanoblast cell line-A / 97

potential treatment modality for vitiligo

Sumathy Babitha1, Jeong-Hyun Shin2, SunA Yoon3, Sang-Joo Park3, Eun-Ki Kim3

1BK21 Center for Advanced Medical Education, Inha University School of Medicine, Incheon;2Department of Dermatology, Inha University School of Medicine, Incheon;3Department of Biological Engineering, Inha University, Incheon, Korea

P-6 Genetic polymorphisms of HLA-F and HLA-G are associated with / 98

susceptibility to non-segmental vitiligo in Korean populations

Lee EJ1, Shin MK1, Hong MS2, Uhm YK,2 Lee MH1

Kohwang Medical Research Institute and Departments of 1Clinical Pharmacology and 2Dermatology,

School of Medicine, Kyung Hee University, Seoul, Korea

P-7 MKK6 increases the melanocyte dendricity through the regulation of / 99

Rho family GTPases

Mi Yoon Kim1, Jin-Hwa Kim1, Tae-Young Choi1, Yu Jin Kim1, Young Lee1, Young Ho Lee2,

Chang Deok Kim1, Jeung-Hoon Lee1, Tae-Jin Yoon3

Department of 1Dermatology, 2Anatomy, School of Medicine, Chungnam National University, Daejeon;3Department of Dermatology, School of Medicine, Gyeongsang National University, Jinju, Korea

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P-8 Detection of Autoantigen of Melanocyte Reacting with Autoantibodies / 100

in Sera of Vitiligo Patients by Proteomics

Ji Young Kim, Jeong Eun Do, Keun Jae Ahn, Sang Ho Oh

Department of Dermatology, Yonsei University College of Medicine

P-9 Adipose-derived stem cell-cultured media improves oxazolone / 101

induced atopic dermatitis skin lesions

Haejin Lee, Minyoung Jung, Eung Ho Choi

Department of Dermatology, Yonsei University Wonju College of Medicine

P-10 Inhibitory Effects of Effective Microoganism Fermentation Substance / 102

(Em-S) on the Development Atopic Dermatitis-Like Skin Lesions in NC/ Nga MICE

Seon Il Jang*, Ji Ye Mok, Kwang-Hyun Park, Na-Na Seong, Ji-Min Park, Jung-Keun Cho,

Ji-Won Choi, and Byung-Eun Moon

Jeonju University Atopy & Health Research Institute, Jeonju, Korea, School of Alternative Medicine &

Health Science, College of Alternative Medicine, Jeonju University, Jeonju, Korea. Department of

Biochemistry, Chonbuk National University Medical School, Jeonju, Korea, Evermiracle research institute,

Jeonju, Korea

P-11 S100A9 correlates with clinical improvement of atopic dermatitis with / 103

immunotherapy

Chang Ook Park1, Ji Yeon Noh2, Sang Ho Oh2, Byung Gi Bae2, Sung Min Noh2,

Kwang Hoon Lee2

1Department of Dermatology, The Armed Forces Byukjae Hospital, 2Department of Dermatology &

Cutaneous Biology Institute, Yonsei University College of Medicine, Seoul, Korea

P-12 Thymic stromal lymphopoietin enhances Th2 cytokine production / 104

by invariant natural killer T cells

Chang Ook Park1, Byung Gi Bae2, Wen Hao Wu2, Sang Ho Oh2, Sung Min Noh2,

Ji Yeon Noh2, Keun Jae An2, Kwang Hoon Lee2

1Department of Dermatology, The Armed Forces Byukjae Hospital; 2Department of Dermatology &


P-13 The effect of relaxation therapy on atopic dermatitis / 105

Byung Gi Bae1, Sang Ho Oh1, Chang Ook Park2, Il Ho Park3, Ji Yeon Noh1, Kwang Hoon Lee1

1Department of Dermatology & Cutaneous Biology Institute, Yonsei University College of Medicine,

Seoul; 2Department of Dermatology, The Armed Forces Byukjae Hospital; 3Department of Psychiatry,

Myongji Hospital, Kwandong University College of Medicine, Gyeonggi, Korea

P-14 Beneficial effects of the conditioned medium of adipose tissue-derived / 106

stem cells on human follicular cells

Chong-Hyun Won1, Seung-Hyun Shin1, Gyeong-Hun Park1, Sung-Eun Chang1, Mi-Woo Lee1,

Jee-Ho Choi1, Kee-Chan Moon

1, Jee-Soo An

2, Oh-Sang Kwon

2, Hyeon-Gyeong Yoo

2,

Soon-Jin Choi2, Kyu-Han Kim2

1Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul;2Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea

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P-15 Changes of integral hair lipid according to intrinsic hair aging / 107

Youn-hee Lee1, Youn-Duk Kim1,2, Sung-Hae Kim1, Tae-Sik Park3, Won-Soo Lee1

1Department of Dermatology and Institute of Hair and Cosmetic Medicine, Yonsei University Wonju

College of Medicine, Wonju; 2Central Research Laboratories of Aekyung industrial Co. Ltd., Daejeon;3Laboratory of Lipid Biology, Lee Gil Ya Cancer and Diabetes Institute, Korea

P-16 Hair growth regulation by the extract of Chrysanthemum Zawadskii / 108

Long-Quan Pi1, Kunhoae Kim2, Jeong-hwan Lee2, Gyeong-Yup Chi2, Xing-Hai Jin1,

Yoon-Hee Lee1, Jae-Hong Ji1, Youn-Duk Kim1, In-Sik Cho2, Won-Soo Lee1


College of Medicine, Wonju; 2Central Research Laboratories of Aekyung industrial Co. Ltd., Daejeon, Korea

P-17 The changes of hair lipid composition after UV irradiation on / 109

three ethnic hairs

Jae Hong Ji1, Youn-Duk Kim1,2, Sung-Hae Kim1, Won-Soo Lee1



P-18 The effects of Ornithine Decarboxylase on human hair growth in vitro / 110

Long-Quan Pi1, Xing-Hai Jin1, Jae-Hong Ji1, Yoon-Hee Lee1, Youn-Duk Kim1,

Sungjoo Tommy Hwang2, Won-Soo Lee1


College of Medicine, Wonju; 2Dr. Hwang’s Hair-Hair clinic, Seoul, Korea

P-19 Epigallocatechin-3-gallate has an anti-inflammatory effect by regulating / 111

macrophage migration inhibitory factor-induced T helper related chemokines and

cytokines in human HaCaT cells

Sun Up Noh, Hei Sung Kim, Hoon Kang, Jun Young Lee, Hyung Ok Kim, Young Min Park

Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea

P-20 Homoisoflavanone prevents allergic responses by blocking degranulation / 112

mast cells through the inhibition of FceRI signaling pathways

Yunsang Lee, Seulgi Hur and Tae-Yoon Kim


The Catholic University of Korea, Seoul Korea

P-21 Effects of corticotropin-releasing hormone on cytokine expression in / 113

T cells

Sang Ho Oh, M.D.1,3, Chang Ook Park, M.D.2,3, Ji Young Kim, MS1, Wen Hao Wu, Ph.D.1,

Kwang Hoon Lee, M.D., Ph.D.1

1Department of Dermatology & Cutaneous Biology Institute, Yonsei University College of Medicine,

Seoul; 2Department of Dermatology, The Armed Forces Byukjae Hospital; 3Both Authors Contributed

Equally to the Study

P-22 The role of ROS produced in XS106 dendritic cells treated by / 114

benzalkonium chloride

Jeong Hwan Je, Dong Hyun Kim, Dashlkhumbe Bayamba, Tae Kyun Kim, Jin Mo Park,

Hyo Jin Noh, Min-Geol Lee

Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine

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P-23 Cigarette smoke-induced Egr-1 regulates the expression of the Cyr61 / 115

in human skin dermal fibroblasts

Ji Na Kim1, Sang Hoon Jeong1, Yoon-Hee Park1, Sang Min Yi2, Jae Hwan Kim2,

Jae Eun Choi2, Il-Hwan Kim2, Young Chul Kye2, Sang Wook Son2

1Laboratory of Cell Signaling and Nanomedicine, Korea University College of Medicine, Seoul;2Department of Dermatology and Division of Brain Korea 21 Project for Biomedical Science, Korea

University College of Medicine, Seoul, Korea

P-24 Expression of Wnt5a, CYR61 and HSP90 in the human skin treated / 116

with ablative fractional resurfacing CO2 laser treatment validated

by gene expression profiling

Oun Jae Park, Hana Bak, Chong Hyun Won, Sung Eun Chang, Mi Woo Lee, Jee Ho Choi,

Kee Chan Moon

Asan Medical Center, Korea

P-25 Horse oil induces the increased expression of IL-10 in HaCaT cells / 117

Sung-Ae Kim, Min-Chul Kang, Jun-Il Kwon, Jae-We Cho, Kyu-Suk Lee


P-26 Simvastatin inhibits transforming growth factor- 1 induced collagenβ / 118

type I and CTGF Expression in keloid fibroblasts

Je-Ho Mun, M.D.1, Young-Mi Kim2, Hyun-Chang Ko, M.D.1, Byung-Soo Kim, M.D.1,

Jae-Ho Kim2, Moon-Bum Kim, M.D.1

Department of 1Dermatology, 2Physiology, School of Medicine, Pusan National University, Busan, Korea

P-27 SOD3 expression up-regulated by PKC-delta inhibits cell proliferation / 119

in melanoma via the Stat1-p21 pathways

Hyun Yoo, Yunsang Lee, Byeongwook Jeon and Tae-Yoon Kim



P-28 Differential expression of ABO antigens in normal and altered skin / 120

conditions

Dong-Hun Lee, Jang Hee Oh, Ji Yong Jung, In Ho Kwon, Se Rah Lee, Yeon Kyung Kim,

Hyun Sun Yoon, Eun Young Seo, and Jin Ho Chung


Aging Research, Clinical Research Institute, Seoul National University Hospital; Institute of Dermatological

Science, Medical Research Center, Seoul National University, Seoul, Korea.

P-29 The role of aryl hydrocarbon receptor on UVB-induced MMP-1 / 121

expression in human skin cells

Jeong Yoon Lee, Chi-Hyun Park, Jang-Hee Oh, Jin Ho Chung


Aging Research, Clinical Research Institute, Seoul National University Hospital; Institute of Dermatological

Science, Medical Research Center, Seoul National University, Seoul, Korea.

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P-30 Investigation of papulopustular eruptions caused by cetuximab / 122

treatment shows altered differentiation markers and increases in

inflammatory cytokines

Gyeong-Hun Park1, Seung-Seog Han2, Mi-Woo Lee1, Jee-Ho Choi1, Kee-Chan Moon1

1Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul;2Dermatology Clinic, Seoul, Korea

P-31 Identification of the filaggrin gene polymorphisms with ichthyosis / 123

vulgaris in Korean patients

Dong Ha Kim1, In Su Kim1, Jin Woong Lee1, Kwang Ho Yoo1, Mi Sook Jeong2,

Kim Eun Joo2, Beom Joon Kim1, Myeung Nam Kim1, Kui Young Park1, Kapsok Li1,

Seong Jun Seo1, Chang Kwun Hong1

Department of Dermatology, Chung-Ang University College of Medicine1, Chung-Ang Medical Research Center2

P-32 The effect of calcipotriol on the expression of Human defensin-2 andβ / 124

LL-37 in cultured human keratinocytes

Woo Sun Jang1, Hyun Kyu Kim1, Juhee Park1, Hye In Lee1, Mi Sook Jeong2, Eun Joo Kim2,

Beom Joon Kim1, Myeung Nam Kim1, Kui Young Park1, Kapsok Li1, Seong Jun Seo1,

Chang Kwun Hong1

1Department of Dermatology, Chung-Ang University College of Medicine, 2Chung-Ang Medical Research Center

P-33 Effect of topical application and intraperitoneal injection of oregonin / 125

on atopic dermatitis (AD) in NC/ Nga mice

Woo Sun Jang1, Hyun Kyu Kim1, Juhee Park1, Hye In Lee1, Mi Sook Jeong2, Eun Joo Kim2,

Beom Joon Kim1, Myeung Nam Kim1, Kui Young Park1, Kapsok Li1, Seong Jun Seo1,

Chang Kwun Hong1

Department of Dermatology, Chung-Ang University College of Medicine1, Chung-Ang Medical Research Center2

P-34 Differential expression patterns of MMPs and their role in the invasive / 126

properties of epithelial premalignant tumors and invasive squamous cell carcinoma

Mi Ryung Roh, M.D.1, Hang Ran Chang, Ph.D.2, Ji Eun Kwon, M.D.1,

Sun-Young Rha, M.D., Ph.D.2, Kee Yang Chung, M.D., Ph.D.1

1Department of Dermatology and Cutaneous Biology Research Institute, Department of Pathology and2Department of Medical Oncology, Yonsei University College of Medicine, Seoul, Korea

P-35 Expression of ATF3 on skin cancer / 127

Myoung-Shin Kim1, Seung-Gyun In2, Hyung-Min Lee1, Chong-Hyun Won1,

Sung-Eun Chang1, Mi-Woo Lee1, Jee-Ho Choi1, Kee-Chan Moon1

1Department of Dermatology, Asan Medical Center, University of Ulsan, College of Medicine,2Department of Dermatology, Inha University Hospital

P-36 Expression of matrix metalloproteinases and their role in the invasive / 128

property of squamous cell carcinoma

Mi Ryung Roh, M.D.1, Jin Young Jung, M.D.1, Su Hyun Lee, M.D.1, Keun-Jae Ahn, Ph.D.1,

Hyun Sook Kim1, Sun-Young Rha, M.D., Ph.D.

2, Kee Yang Chung, M.D., Ph.D.

1

Department of 1Dermatology and Cutaneous Biology Research Institute, 2Medical Oncology, Yonsei


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P-37 Association of thymic stromal lymphopoietin gene -847C>T / 129

polymorphism in generalized vitiligo

Kyung Ah Cheong1, Soo-Cheon Chae2, Yong-Shin Kim3, Hyok Bu Kwon1,

Hun-Taeg Chung3 and Ai-Young Lee1

1Department of Dermatology, Dongguk University Ilsan Hospital, Goyang, Korea2Department of Pathology, School of Medicine, Wonkwang University, Iksan, Chonbuk, Korea;3Genome Research Center for Immune Disorders, School of Medicine, Wonkwang University, Iksan,

Chonbuk, Korea

P-38 Expressions of NOTCH signaling pathway in psoriasis / 130

Chang Sung Eun1, Moon Kee Chan1, Choi Jee Ho1, Lee Mi Woo1,

Won Chong Hyun1, Chang Deok Kim2, Seung Hyun Bang1

1Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine,2Department of Dermatology, School of Medicine, Chungnam National University

P-39 Sphingosylphosphorylcholine-induced interleukin-6 production is / 131

mediated by protein kinase C and p42/ 44 extracellular signal-regulated

kinase in human dermal fibroblasts

Dae-Kyoung Choi1, Kyung-Cheol Sohn1, Yoo Bin Kwon1, Nari Kim1, Ah Young Cho1,

Young Ho Lee2, Tae-Jin Yoon3, Young Lee1, Chang Deok Kim1, Jeung-Hoon Lee1

1Department of Dermatology, School of Medicine, Chungnam National University, Daejeon;2Department of Anatomy, School of Medicine, Chungnam National University, Daejeon;3Department of Dermatology, School of Medicine, Gyeongsang National University, Jinju, Korea

P-40 Alteration of extracellular matrix modulators in photoaged skin after / 132

combined laser, light and radiofrequency treatment

Chae Hwa Kim, Jeong Eun Kim, Gyeong Hun Park, Chong Hyun Won,

Sung Eun Chang, Mi Woo Lee, Jee Ho Choi, Kee Chan Moon

Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine

대한피부연구학회 회칙 / 133

대한피부연구학회 연혁 / 136

현임원진 / 141

Symposium

Past Positions

1985-1987 Instructor, Gyungsang National University College of Medicine

1987-1990 Served in Korean Army

1991-1996 Instructor and Assistant Professor, Seoul National University College of Medicine

1993-1995 Visiting Scientist, National Institute of Dental Research, NIH, USA

1996-2001 Associate Professor, Seoul National University College of Medicine

Educations

1974-1980 Pre-medical and Medical School (M.D.), Seoul National University College of Medicine

1981-1986 Graduate School (Ph.D. in Medicine), Seoul National University

1980-1984 Resident training for Pathologist, Seoul National University Hospital

Certificates

Medical Doctor (Korean licence No. 21857, Feb. 1980)

Korean Board of Pathology (licence No. 186, Apr. 1984)

Toxicologic Pathologist (licence No. 35. May, 2003)

Member

American Association of Cancer Research (1995- )

National Cancer Control Program Committee, Korea (1996-2004)

Editorial Board

Human Pathology (2008- )

Korean Journal of Pathology (2002- )

Cancer Research and Treatment (Associate Editor, 2005- )

Woo Ho Kim, M.D., Ph.D.Department of Pathology, Seoul National University College of Medicine

Seoul, Korea

CURRICULUM VITAE

- 18 -

The epithelial cells are characterized by polarized cells which normally interact with basement

membrane via their basal surface. The mesenchymal cells have the ability of migratory capacity,

invasiveness, elevated resistance to apoptosis and increased production of extracellular components.

In many physiologic and pathologic conditions, the epithelial cells lose their own capacity and

obtain mesenchymal characteristics. This phenomenon is called as epithelial-mesenchymal transition

(EMT) and is drived by activation of transcription factors, expression of specific cell-surface proteins,

re-organization and expression of ECM-degrading enzymes, and changes in the expression of

specific micro RNAs.

Three different subtypes of EMT are encountered in different biologic settings. Type 1 EMT is

associated with implantation and embryonic gastulation, and give rise to the mesoderm and

endoderm. Type 2 EMT occurred in inflammation and fibrosis. It is expressed over extended period

of time and can eventually destroy an affected organ. Type 3 EMT represent the transformation

of epithelial cancer cells capable of invasion and metastasis. While the outcome of the above three

types of EMT in the generation of motile cells of mesenchymal phenotype, the mecharism of EMT

is different. Future research will focus on uncovering the molecular similarity and difference

among EMT programs in three different settings.

S-1

Epithelial-Mesenchymal Transition (EMT),

an overview

Woo Ho Kim

Department of Pathology, Seoul National University College of Medicine, Seoul, Korea

- 19 -

Education

1982-1984 Pre-medical Course, Ewha Women's University, College of Medicine, Seoul, Korea

1984-1988 M.D., Ewha Women's University, College of Medicine, Seoul

Feb. 1992 Master of Medicine, Graduate School of Ewha Women's University, College of

Medicine, Seoul

Aug. 1995 Ph.D., Graduate School of Ewha Women's University, College of Medicine, Seoul

Postgraduate Training & Employment

Mar. 1989-Feb. 1993 Residency of Internal Medicine, Ewha Women's University Hospital,

Seoul

Mar. 1993-Feb. 1994 Clinical Fellow of Nephrology, Department of Internal Medicine,

Severance Hospital, Yonsei University, College of Medicine, Seoul

Mar. 1994-Feb. 1995 Clinical Fellow of Nephrology, Department of Internal Medicine

Ewha Women's University Tongdaemun Hospital, Seoul

Mar. 1995-Feb. 1997 Fulltime Instructor, Department of Internal Medicine, Ewha Women's

University, College of Medicine, Seoul

Mar. 1997-Feb. 2003 Assistant Professor of Medicine, Department of Internal Medicine Ewha

Women's University, College of Medicine, Seoul

Jun. 1999-Jul. 2000 Research Fellow, Division of Nephrology, University of Washington

Seattle, WA, USA

Aug. 1999-Jun. 2001 Research Fellow, Division of Nephrology, Baylor College of Medicine,

Houston, TA, USA

Mar. 2003-Feb. 2008 Associate Professor of Medicine, Department of Internal Medicine,

Ewha Women's University, College of Medicine, Seoul

Mar. 2008-present Professor of Medicine, Department of Internal Medicine, Ewha Women's

University, College of Medicine,

Licenses and Qualification

1988 Doctor of Medicine and License of General Medicine-KOREA (licence no. : 36200)

1992 Board Certification in Internal Medicine-KOREA (licence no. : 3516)

1997 Subspecial Board Certification in Nephrology-KOREA (no : 5-97-150)

1998 Dialysis Specialist, Korean Society of Nephrology

Duk-Hee Kang, M.D., Ph.D.Department of Internal Medicine, Ewha Women's University Mokdong Hospital,

Seoul, Korea

CURRICULUM VITAE

- 20 -

Honors & Awards

Feb. 1988 Summa cum laude

Ewha Women's University, College of Medicine. Honored student award

May 1995 Best Abstract Award, Korean Society of Nephrology

(Title: Changes in plasma endothelin concentration and hemodynamic parameters

during rHuEpo administration in maintenance hemodialysis patients)

May 1996 Best Abstract Award, Korean Society of Nephrology

(Title: Anticardiolipin antibody and lupus anticoagulant : Association with vascular

access occlusion in hemodialysis patients)

Jun. 1997 Congress Award, European Dialysis & Transplantation Association

Oct. 2001 Best Poster, ISN Fellow Forum, 2001 ASN Meeting

May 2002 “Best Doctor” Award, Ewha Medical Center

May 2003 Chung-Ram Award, Korean Society of Internal Medicine

May 2004 Young Investigator Award, Korean Society of Nephrology

Oct 2004 Wunsch Medical Prize, Young Investigator Award, Korean Medical Association

Oct 2006 Basic Research Award, Korean Association of Woman Doctors

Research Funds Received (current)

Mar. 2007~ Kureha Research Grant, Kureha, Japan

(Title: Effect of AST-120 on hyperuricemia and renal disease progression)

Mar. 2008~ Basic Research Grant, Korea Science & Engineering Foundation

(Role of ER stress in acute and chronic kidney disease)

May 2008~ Interventional Research Grant, Ministry of Health & Welfare

(Title: ER stress and endothelial dysfunction)

Recent Invited Talks at the International Meeting

2008 Asian Pacific Congress of Nephrology, Kuala Lumpur, Malaysia

“Uric acid as a novel risk factor of cardiovascular disease in CKD patients”

2008 Asian Congress of Pediatric Nephrology, Bangkok

“VEGF and its receptors in chronic kidney disease”

2009 World Congress of Nephrology, Milan, Italy

“Role of vascular disease as a culprit of progression of renal disease”

Membership

American Society of Nephrology

International Society of Nephrology

European Dialysis and Transplantation Association

Korean Association of Internal Medicine (Scientific and Publishing Committee)

Korean Medical Association

Korean Society of Nephrology (Scientific, Publishing and Collaborative Committee)

Korean Society of Biochemistry and Molecular Biology

Korean Society of Hypertension

- 21 -

Recent evidences demonstrate a key role of cell plasticity in the process of wound healing, tissue

regeneration, and organ fibrosis. Epithelial-to-mesenchymal transition (EMT) is a paradigmatic

process of cell plasticity, which leads epithelial cells to lose their polarization and specialized

junctional structures, to undergo cytoskeleton reorganization, and to acquire morphological and

functional features of mesenchymal-like cells with an expression of migratory phenotype. Although

EMT is a critical and physiologic process in embryogenesis and tissue repair, it can impose

unfavorable effect by promoting tissue fibrosis in non-physiologic conditions. In human disease

as well as several animal models of wound repair or organ fibrosis, an EMT has been found to

be triggered by microenvironmental changes such as local inflammation, oxidative stress or

hypoxia, and cease once trigger signal is attenuated. In the setting of organ fibrosis, EMT can

continue to respond to ongoing stimuli leading eventually to organ destruction. Among various

cytokines modulating the process of EMT, transforming growth factor-β (TGF- ) plays a pivotalβ

role in mediating the phenotypic transition mainly via Smad-dependent pathway. To orchestrate

healthy wound healing, both EMT and MET, which is a reverse process of EMT to convert

mesenchymal cells to cells with epithelial phenotype, are necessary at each stage of wound repair.

MET is now regarded as a novel therapeutic target to inhibit organ fibrosis and to promote healthy

wound repair with an identification of several candidates of therapeutic intervention including

hepatocyte growth factor (HGF) or bone morphogenic peptide-7 (BMP-7). There are also preliminary

evidences of an involvement of numerous downstream signaling cascades such as SGK-1, Best1,

IGF-1, Smurf 2 or SnoN in the development of EMT and MET. Strategies to disrupt any one of

these may also negate EMT and prevent fibrotic scar formation in multiple organs including skin.

S-2

EMT and wound healing

Duk-Hee Kang, M.D., Ph.D.

Division of Nephrology, Ewha Womans University School of Medicine, Seoul, Korea

- 22 -

Educational Background

1988. 2. Graduated from College of Medicine, Seoul National University, Korea

1988. 2. Degree of Medical Doctor (M.D.), Korea

1992. 2. Degree of Ph.D. (Microbiology) from College of Medicine, Seoul National University, Korea

Career

1988. 3-1992. 2 Teaching and Research Assistant in Department of Microbiology, College of

Medicine, Seoul National University, Korea

1992. 3-1992. 5 Training for Military Personel (National obligation)

1992. 5-1995. 5 Medical Officer in National Institute of Health in Korea (National obligation)

1995. 5-1997. 9 Instructor in Hallym University, Korea

1997. 9-1998. 8 Assiatant Professor in Hallym University, Korea

1998. 9-2002. 2 Visiting Fellow at Skin Biology Lab NIAMS/NIH

2002. 3-2007. 2 Associated Professor in Korea University

2007. 3-present Professor in Korea University

Sun Ho KeeAssociate Professor, Lab of Epithelial Cell Biology, College of Medicine, Korea University,

Seoul, Korea

CURRICULUM VITAE

- 23 -

Microtubules (MT) are involved in numerous cellular functions including maintenance of cell

shape, cell migration and intracellular transport. This functional diversity may be rooted in

structural diversity of MTs. Alpha-/beta-tubulin which are components of MT have several

isotypes and are modified post-translationally, which may resulted in structural heterogeneity.

Among beta-tubulin isotypes, class II tubulin has several unique features. Class II tubulin localizes

in nuclei and peri-centrosome. In addition, class II tubulin expression is regulated transcriptionally

according to various cellular contexts.

Herein, regulation of class II tubulin expression in several skin cells will be presented. First,

up-regulated class II tubulin expression could be observed in granular layer of skin epidermis

and cultured differentiating keratinocytes. But this expression abruptly disappeared in terminally

differentiating keratinocytes (cornified layer). Second, in hair follicle cells, class II tubulinexpression

is specifically upregulated in cells of germinal matrix cell (GMC) origin but not in bulge-derived

cells. Third, melanocytes strongly expressed class II tubulin but malignant melanoma showed

reduced expression. To explore negative role of class II tubulin in malignant melanoma development,

we transfected class II tubulin cDNA and established class II expressing clones (B16-clII) from B16

cells which has low level of class II expression. These B16-clII cells showed reduction of cell

proliferation, colony forming ability in soft agar, and tumerigenic potential in mice, suggesting

of inverse relationship between class II tublin expression and malignancy.

Conclusively, our results suggested that class II tubulin expression is variably regulated

according to cell types and may be useful for diagnosis of differentiati-related skin diseases.

S-3

Differentiation-related expression of

class II beta-tubulinin skin

Sun Ho Kee

Department of Microbiology, College of Medicine, Korea University, Seoul, Korea

Invited Lectures

Education/Training

1983 M.D. Medicine Ehime University Medical School (Japan)

1988 Ph.D. Immunology Osaka University Graduate School of Medicine

1988-92 Postdoc Immunology Albert Einstein Medical College

Positions

Since 2007 Professor of Dermatology, Kochi Medical School, Kochi University

2006-2007 Associate Professor, Department of Dermatology, Osaka University Medical School

2005-2006 Assisstant Professor, Department of Dermatology, Osaka University Medical School

2004-2005 Director of Dermatology, Sumitomo Hospital, Osaka

2003-2004 Visiting Assisstant Professor, Department of Carcinogenesis, MD Anderson Cancer Center

1994-2003 Assisstant Professor, Department of Dermatology, Osaka University Medical School

1992-1994 Clinical Director of Dermatology, Sakai Municipal Hospital, Osaka

1983-1984 Resident in Osaka University Hospital (Dermatology).

Honors and Award

2009 ESDR Poster Award

2008 Rohto Award

2006 Japanese Society of Investigative Dermatology (JSID) Award

2005 Eugene Farber Award

2001 Galderma Award

2000 Minami Award (Best research award for dermatology in Japan)

Publications

Selected list of peer-reviewed publications and review articles

1. Sano S, Chan KS, Digiovanni J. Impact of Stat3 activation upon skin biology: A dichotomy of its role between

homeostasis and diseases. J Dermatol Sci 50: 1-14, 2008

2. Chan KS, Sano S, Kataoka K, Abel E, Carbajal S, Beltran L, Clifford J, Peavey M, Shen J, Digiovanni J. Forced

expression of a constitutively active form of Stat3 in mouse epidermis enhances malignant progression of

skin tumors induced by two-stage carcinogenesis. Oncogene 40: 40-45, 2008

3. Sano S, Chan KS, Carbajal S, Clifford J, Peavey M, Kiguchi K, Itami S, Nickoloff BJ, DiGiovanni J. Stat3

links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic

mouse model. Nat Med 11: 43-9, 2005

Shigetoshi SanoProfessor of Dermatology,

Kochi Medical School, Kochi University, Japan

CURRICULUM VITAE

- 28 -

Psoriasis is characterized by excessive growth and aberrant differentiation of keratinocytes, and

considered to be an immune-mediated complex multigenic disease. Experiments using animal

models revealed that the development of psoriasis requires the interaction of keratinocytes and

immunocytes. Since cyclosporine A was introduced to be a "gold standard therapy" for severe

psoriasis, the critical role for activated T cells emerged. Thelper 17 (Th17) cells are a newly identified

T cell subset because of their producing IL-17, distinct from Th1 and Th2, and have been implicated

in the pathogenesis of psoriasis. Th17 cells produce a variety of cytokines, including IL-17A, IL-17F,

and IL-22. IL-22 was proved to mediate acanthosis through the activation of keratinocytes Stat3

in vivo. A number of studies have demonstrate that psoriatic lesion showed increased mRNAs

of aforementioned Th17 cytokines as well as IL-23, which plays a critical role in maturation and

activation of Th17. These results clearly indicated that IL-23/Th17 represents a key axis for the

pathogenesis of psoriasis, as well as the therapeutic efficacy of anti-IL-12/23p40. We have

established a psoriasis model mouse by introducing a constitutive active Stat3 transgene under

the keratin 5 promoter (K5.Stat3C). To examine whether the IL-23/Th17 axis was necessary for

the development of skin lesions of these mice, we administrated them with anti-IL-12/23p40 (gift

from Centocor Reseach & Development, Inc.) or crossed them with IL-17A knockout mice (gift

from Dr. Iwakura). Psoriasiform lesion in K5.Stat3C mice required IL-23 to develop the psoriasis-

like skin lesions, and transcript levels of Th17 cytokines including IL-22, and epidermis-derived

psoriasisassociated genes were apparently downregulated following anti-IL-12/23p40 or anti-IL-

23p19 treatment. However, IL-17A deficiency in K5.Stat3C mice demonstrated a partial ameliora-

tion of skin phenotype, on which anti-IL-12/23p40 treatment was further effective.

Thus, our results implicated that the pathogenesis of psoriasis in this model is dependent on

the IL-23/Th17 axis but partially on IL-17A itself.

IL-1

Recent Progress in Psoriasis Research on Mechanistic

Interaction Between Cytokines and Keratinocytes:

A Distinct Role of the IL-23/ Th17 Axis

Shigetoshi Sano

Kochi Medical School, Kochi University, Japan

- 29 -

Education and Training

1980-1986 M.D. in Medicine, China Medical University

1991-1996 Ph.D. in Dermatology and Venereology, China Medical University

1999-2000 Visiting research fellow in Department of Dermatology, University Medical Center

Benjamin Franklin, the Free University of Berlin, Germany

Professional Experience

1986-2002 Resident/Lecturer, Assistant, Associate Professor, Dept of Dermatology, No.1 Hospital

of China Medical University

1999-now Vice Chairman, Key Laboratory of Immunodermatology, Ministry of Health, China

2002-now Professor, Dept of Dermatology, No.1 Hospital of China Medical University

2002-now Chairman, Dept of Dermatology, No.1 Hospital of China Medical University

Professional Societies

2009-now Vice President, the Chinese Society of Dermatology

2005-now President, Dermatovenereological Association, Liaoning Branch, the Chinese Medical

Association

2004-2008 Council Member of Asian Dermatological Association

Chun-Di He, M.D., Ph.D.Professor and Chairman, Department of Dermatology, No.1 Hospital of China Medical

University, 155 N. Nanjing Street, Shenyang, Liaoning110001, China

CURRICULUM VITAE

- 30 -

In humans and mice, the hairless (HR) transcription factor is essential for maintaining hair, but

not for making it. In HR-deficient skin, which results from recessive HR mutations, hair follicles

develop normally and produce normal, visible hair. But after completing this initial round of hair

production, the follicles self-destruct and never regenerate, resulting in total, permanent baldness.

Marie Unna hereditary hypotrichosis (MUHH) is an autosomal dominant form of genetic hair

loss. In a large Chinese family carrying MUHH, we identified a pathogenic initiation codon

mutation in U2HR, an inhibitory upstream ORF in the 5 UTR of the gene encoding the human

hairless homolog (HR). 13 different MUHH associated Mutations was identified, all of which share

a particular property: they lie within an upstream ORF (uORF) present in the HR transcript and

52 to the HR ORF (the HR coding sequence). uORFs appear in many mRNAs, especially those

encoding regulators of cell growth, and are known to serve as translational repressors. U2HR is

predicted to encode a 34-amino acid peptide that is highly conserved among mammals. In 18 more

families from different ancestral groups, we identified a range of defects in U2HR, including loss

of initiation, delayed termination codon and nonsense and missense mutations. Functional analysis

showed that these classes of mutations all resulted in increased translation of the main HR

physiological ORF. Our results establish the link between MUHH and U2HR, show that fine-tuning

of HR protein levels is important in control of hair growth, and identify a potential mechanism

for preventing hair loss or promoting hair removal.

These mutations seem to disrupt an unusual leader sequence-based mechanism of translational

repression, making MUHH the first example of a disease linked to this form of repression. Such

findings have opened new windows into HR function and regulation and are certain to inspire

studies of HR in the years ahead.

IL-2

Hair Loss in Translation: What Can We Learn

from the Recent Studies on Marie Unna

Hereditary Hypotrichosis

Chun-Di He, M.D., Ph.D.

Department of Dermatology No. 1 Hospital of China Medical University; Key Laboratory of

Immunodermatology, Ministry of Health (China Medical University) Shenyang 110001, China

- 31 -

Education

1998 Ph.D., University of Tokyo (Thesis: The function of transcription factor Sp3 in the transcriptional

regulation of the human 2(I) collagen gene)α

1990 M.D., University of Tokyo

Professionla Training and Emplyment

2005-present Professor & Chairman, Department of Dermatology & Plastic Surgery, Faculty Life

Sciences, Kumamoto University, Kumamoto, Japan

2005 Associate Professor, Department of Dermatology, Faculty of Medicine, University of

Tokyo, Tokyo, Japan

2001-2005 Lecturer, Department of Dermatology, Faculty of Medicine, University of Tokyo,

Tokyo, Japan

1997-2001 Assistant, Department of Dermatology, Faculty of Medicine, University of Tokyo,

Tokyo, Japan

1994-1997 Research Fellow, Division of Rheumatology & Immunology, Medical University of

South Carolina, SC, USA


Tokyo, Japan

1992-1993 Clinical Fellow, Department of Dermatology, Kanto Rosai Hospital, Kanagawa, Japan

1991-1992 Clinical Fellow, Department of Dermatology, Kousei General Hospital, Tokyo, Japan


Tokyo, Japan

Societies

Japanese Society of Dermatology, Japanese Society of Investigative Dermatology, Japanese Society

of Clinical Immunology, Japanese Society of connective tissue Research, American Academy of

Immunologists, American Society for Matrix Biology, Japanese Society of Allergy, Japanese Society

of Rheumatology, Japanese Society of Cosmetic Dermatology, Japanese Society of Psoriasis, Japanese

Society of Skin Cancer

Awards

2006 Japan Rheumatism Foundation Award

2005 Japanese Society of Investigative Dermatology Award

2001 Japanese Society of Connective Tissue Research Award

Hironobu IhnDepartment of Dermatology & Plastic Surgery, Faculty Life Sciences, Kumamoto University,

Kumamoto, Japan

CURRICULUM VITAE

- 32 -

Fibrosis is a complex biological process involving an acute inflammatory response. Transient

activation of fibroblasts to proliferate and produce elevated quantities of extracellular matrix, such

as type I collagen, is essential to fibrosis. Transient fibroblast activation is likely regulated by a

variety of cytokines, such as TGF- . We have investigated the transcriptional regulation and signalβ

transduction of 2(I) collagen gene. Moreover, we have shown the involvement of autocrine TGF-α β

signaling in the pathogenesis of fibrosis, especially in systemic sclerosis, which is mediated by

overexpression of TGF- receptors, integrin v 5, and thrombospondin-1 on the activatedβ α β

fibroblasts.

IL-3

Molecular mechanism of fibrosis

Hironobu Ihn, M.D., Ph.D.

Department of Dermatology & Plastic Surgery, Faculty of Life Sciences, Kumamoto University,

Kumamoto, Japan

- 33 -

Education

1977-1983 M.D. Yonsei University College of Medicine

1983-1985 M.S. Yonsei University College of Medicine

1988-1991 Ph.D. Yonsei University College of Medicine

Training Courses and Employment

1983-1984 Assistant Instructor, Department of Microbiology, Yonsei University, College of Medicine

1985-1988 Visiting Scientist, Laboratory of Microbiology, National Institutes of Health in

Bethesda, Maryland, USA

1989-1992 Resident (Dermatology), Gangnam Severance Hospital

1992-1995 Research Fellow, Department of Dermatology, Yonsei University College of Medicine

1995-2005 Assistant Professor, Department of Dermatology, Yonsei University College of Medicine

2001 Visiting Fellow, Laboratory for Investigative Dermatology, Rockefeller University, New

York, USA

2005-2009 Associate Professor, Department of Dermatology, Yonsei University College of Medicine

Societies

2001-2003 The Korean Dermatological Association, Medical Insurance

2003-2005 The Korean Society for Psoriasis, Director of Publication

2005-2007 The Korean Society for Investigative Dermatology, Academic affairs

2005-2006 The Korean Society for Psoriasis, Treasurer

Wook Lew, M.D., Ph.D.Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea

CURRICULUM VITAE

- 34 -

The Increased Expression of Matrix Metalloproteinase-9

Messenger RNA in the Non-lesional Skin of Patients with

Large Plaque Psoriasis Vulgaris

Wook Lew

Department of Dermatology and the Cutaneous Biology Research Institute,

Yonsei University College of Medicine, Seoul, Korea

A difference of the interleukin-18 (IL-18) mRNA expression among several proinflammatory

genes was previously observed between large plaque (LP) psoriasis patients (more than 5 cm lesions

are typical) and small plaque (SP) psoriasis patients (1~2 cm lesions are typical). Therefore, it is

necessary to test whether there is any difference in the expression of the genes that activate IL-18

or the expression of genes that are induced by IL-18. To test the differential mRNA expressions

of caspase-1, STAT-6, MMP-1, -2, -9 and TIMP-1 according to the clinical types of psoriasis vulgaris

lesions in Korean patients, we have analyzed the skin samples of psoriasis vulgaris patients. The

total cellular RNA of skin samples from groups of patient with LP and SP psoriasis was analyzed

by performing real-time PCR to compare the differences in the mRNA expressions. The caspase-1

and STAT-6 mRNA expression levels from the SP lesional skin of the patients were increased

compared with the caspase-1 and STAT-6 mRNA expression levels from SP non-lesional skin or

normal skin, but these expression levels from the SP non-lesional skin were not significantly

different from those of the LP non-lesional skin. Among MMP-1, -2, -9 and TIMP-1, the expressions

of MMP-1, MMP-2 and MMP-9 mRNA were increased in the SP lesional skin compared with those

of the SP non-lesional skin. The MMP-1 mRNA expressions in both the LP and SP lesional skin

were increased compared with those in the normal skin. The MMP-9 mRNA expression in the

LP non-lesional skin was elevated compared with the MMP-9 mRNA expression in the SP

non-lesional skin (p=0.047). The TIMP-1 mRNA expression levels from the non-lesional skin and

the lesional skin of the psoriasis patients and the normal skin samples were not significantly

different. The increased expression of MMP-9 mRNA in the LP non-lesional skin compared to that

of the SP non-lesional skin in the psoriatic skin suggests that the increased MMP-9 mRNA

expression is related to the large size type of lesion.

UAM Award Lecture

Plenary Lectures

- 37 -

Education

Graduate: University of Michigan Medical School

Ann Arbor, Michigan

Degree: M.D., June 1987

University of Michigan School of Public Health

Ann Arbor, Michigan

Health Degree: M.P.H. in Epidemiology, August 1982

Postgraduate Training and Education

1991 Longwood Chief Resident (Brigham & Women’s, Beth Israel,

Boston Children’s, Dana Farber Hospitals) Department of

Dermatology, Harvard Medical School, Boston, Massachusetts

1988-1992 Residency, Department of Dermatology, Harvard Medical School

Massachusetts General Hospital, Boston, Massachusetts

1989-1990 Research Fellowship, Department of Dermatology, Harvard Medical School

Massachusetts General Hospital, Boston, Massachusetts

1987-1988 Internship, Department of Internal Medicine, University of Rochester

Strong Memorial Hospital, Rochester, New York

Academic Appointment

2008-present Noxell Professor & Chair, Department of Dermatology Johns Hopkins Medicine

2008 Arthur C. Curtis Professor of Dermatologic Translational Research University of

Michigan Medical School

2004-2008 Professor (with tenure), Department of Dermatology University of Michigan, Medical

School

1998-2004 Associate Professor (with tenure), Department of Dermatology University of Michigan

Medical School

1992-1998 Assistant Professor, Department of Dermatology University of Michigan Medical

School

Honors and Awards

2006 Instructional Development Fund Award, Center for Research on Learning and

Teaching, University of Michigan

Sewon Kang, M.D.Department of Dermatology, Johns Hopkins School of Medicine, Baltimore, MD, USA

CURRICULUM VITAE

- 38 -

Society for Investigative Dermatology, Galderma Acne Research Award

2005, 2007 University of Michigan Medical School TAMS Award

1998, 2004 University of Michigan Medical Student Award for Teaching Excellence

2003, 2004, 2006 & 2007

Finalist, Pre-Clinical Kaiser Permanente Award for Excellence in Teaching

2001 University of Michigan Medical School Achievement in Clinical Research Award

Grants

Selected Previous Grant Support

National Institutes of Health & National Center for Research Resources

(UL1RR024986 / KL2RR024987 / TL1RR024988)

“University of Michigan Clinical and Translational Science Award (UM CTSA)”

PI: Dan Clauw, MD

Program Director for Predoctoral Training Grant (TL1): Sewon Kang, MD

2007-2012 Total cost: $54,619,564

National Institutes of Health (R01 AG25186)

“Collagenase degradation of extracellular matrix in aging”

PI: Gary J Fisher, PhD

Co-Investigator: Sewon Kang, MD

2006-2011 Total cost: $1,710,000

Scientific Activities

2008-present Director, Cutaneous Translational Research Program (CTReP)

Department of Dermatology, Johns Hopkins School of Medicine, Baltimore, Maryland

Memberships in Professional Society

since 2004 American Dermatological Association

since 1998 Korean Society for Psoriasis Research, Honorary Member

since 1996 Korean-American University Professors Association

since 1996 American Society for Clinical Pharmacology and Therapeutics

since 1996 National Psoriasis Foundation

since 1994 Dermatology Foundation

since 1993 Inflammation Research Association

since 1993 Skin Pharmacology Society

since 1993 Michigan Dermatological Society

since 1992 Korean Dermatologic Association of America

since 1992 American Academy of Dermatology

since 1992 Society for Investigative Dermatology

since 1989 American Federation for Medical Research

since 1988 Harvard House Officer’s Club

- 39 -

National and International Committees and Responsibilities

Society for Investigative Dermatology

2008-present Member, Executive Committee

2006-present Member, Committee on Finance

2005-present Board of Directors

Dermatology Foundation

2005-present Board of Trustees

The Photomedicine Society

2006-present President-Elect


American Acne & Rosacea Society

2005-present Chair, Scientific Committee


American Academy of Dermatology 2007-2011

2008-present Member, Guidelines/Outcomes Task Force on Atopic Dermatitis Member,

Committee on Research

Korean Dermatologic Association of America

1999-present President

American Dermatological Association

2009-present Member, Audit committee

Journal Reviewer

since 2007 Translational Research

since 2006 American Journal of Pathology

since 2006 Journal of the European Academy of Dermatology

since 2005 Journal of Immunology

since 2004 The FASEB Journal

since 2004 Journal of Cutaneous Medicine & Surgery

since 2002 New England Journal of Medicine

since 2002 Journal of Photochemical and Photobiological Sciences

since 2002 Experimental Dermatology

since 2001 Pediatric Dermatology

since 2001 The Medical Letter on Drugs and Therapeutics

since 2000 Photochemistry and Photobiology

since 2000 Photodermatology, Photoimmunology & Photomedicine

since 1999 Journal of Dermatological Treatment

since 1998 Skin Pharmacology

since 1998 Dermatology (Basel, Switzerland)

since 1998 British Journal of Dermatology

since 1997 Journal of Investigative Dermatology

since 1992 Journal of the American Academy of Dermatology

since 1989 Archives of Dermatology

- 40 -

Editorial Responsibilities

1997-present Member, Editorial Board, Journal of the American Academy of Dermatology

1997-present Member, Editorial Board, Clinical Dermatology (Seoul)

2009-present Member, Editorial Board, Photodermatology, Photoimmunology & Photomedicine

Grant Reviewer

2001-present National Institutes of Health,

a. National Institute of Arthritis and Musculoskeletal and Skin Diseases

1. Special Emphasis Panel for MCRC applications

2. Biomarkers for Rheumatic and Skin Diseases

3. Special Emphasis Panel for K23 Career Development Award

4. Special Emphasis Panel for Dermatomyositis Clinical Trials

5. Chairperson for Special Emphasis Panel for K24 Midcareer Investigator Award

6. Special Emphasis Panel for Loan Repayment Program

7. Hyperaccelerated Awards/mechanisms in Immunomodulation Trials

8. R03, Special Emphasis Panel

b. National Center for Complementary and Alternative medicine

Certification and Licensure

Diplomate, American Board of Dermatology 1992

(recertified until: 2013)

Diplomate, National Board of Medical Examiners 1988

Administrative Positions

Johns Hopkins Department of Dermatology

2008-present Noxell Professor and Chairman

Johns Hopkins Medicine

2009-present Committee on the Promotion of Academic Clinicians

2009-present Agenda Committee of the Advisory Board of the Medical Faculty

- 41 -

Photoaging, premature skin aging that results as a consequence of excessive ultraviolet irradia-

tion, is a well recognized condition now. The notion that photoaged skin can be improved

medically was first realized with topical retinoic acid (RA). Initially it was unclear whether the

action of RA was pharmacologically specific, or was secondary to almost inseparable irritant

reaction. Based on careful clinical and molecular studies, RA-induced effacement of wrinkles has

been correlated with profibrotic cytokine (TGF- , CTGF) formation with subsequent activation ofβ

fibroblasts. With advances in procedural treatments for photoaging, the importance of wound

healing response to skin insult became evident. To date, carbon dioxide laser resurfacing, when

performed correctly, offers the most impressive improvement in photoaged phenotype. More

selective lasers which stimulate the skin in a limited manner, and dermabrasive methodologies

similarly deliver varying degrees of improvement. Even topical 5-FU which can irritate photoaged

skin as it preferentially treats actinic keratosis is credited with delivering improvement to

photoaging. More recent demonstration with cross-linked hyaluronic acid injection inducing

procollagen synthesis points to another mechanism (stretch) to “awaken” fibroblasts. All these

findings suggest that activation of fibroblast is central to successful effacement of wrinkles in

photoaging, and it can occur directly or indirectly, as long as subsequent neocollagen synthesis

ensues.

PL-I

Improving photoaged skin with lasers, dermabrasions

and topical 5-FU: In search of an unifying principle

Sewon Kang, M.D.

Department of Dermatology, Johns Hopkins School of Medicine, Baltimore, MD, USA

- 42 -

Premature skin aging from chronic ultraviolet irradiation, aka photoaging, has been a subject

of great interest by many investigative dermatologists. We now appreciate that in the dermal form

of photoaging (wrinkle formation), UV-induced matrix destruction by matrix metalloproteinases

(MMPs) and concurrent inhibition of procollagen formation are important pathophysiologic events.

Scleroderma (idiopathic or GVHD-associated), hypertrophic scars and keloids are examples of

fibrotic skin conditions with excessive collagen deposition. Although their central pathogenic

mechanisms vary, a way to soften each fibrotic process would be to degrade the matrix (via MMPs)

and block the procollagen synthesis. Therefore, UV radiation is ideally suited to cause antifibrosis

in human skin. As a therapeutic modality, factors to consider are erythemogenic potential,

melanogenic efficiency and the degree of pigmentation in the fibrotic areas. In addition, attenuation

of MMP expression by repeated UV irradiation must be considered in devising a rational

phototherapy regimen. When these variables are properly evaluated, an evidence-based treatment

plan can be formulated to improve skin fibrosis.

PL-II

Harnessing ultraviolet light to improve skin fibrosis

Sewon Kang, M.D.

Department of Dermatology, Johns Hopkins School of Medicine, Baltimore, MD, USA

Research in

Industry

- 45 -

Education

1989-1993 B.FS. Pharmacy, Seoul National University, Seoul, Korea

1993-1995 M.S. Pharmacy/Pharmacology, Seoul National University, Seoul, Korea

2001-2006 Ph.D. Molecular and Systems Pharmacology and Toxicology, Division of Biological

Engineering, Massachusetts Institute of Technology (MIT), USA

Professional Activities

1995-2001 Drug Discovery Division (’95-’99), Skin Research Division (’99-’01), Pacific Corporation

2006 Postdoctoral Associate, Division of Biological Engineering, MIT

2006-2008 Principal investigator/Manager, Biosystems Research, Amorepacific Corporation

2009-present Principal investigator/Manager, Skin Research, Amorepacific Corporation

2009-present Associate editor, Biomolecules & Therapeutics (SCIE-indexed and peer-reviewed

international journal, the official journal of Korean Society of Applied Pharmacology)

Selected Publications

1. Hyun Choi, Shinhyoung Kim, Hyoung-June Kim, Kwang-Mi Kim, Chang-Hoon Lee, Jennifer H. Shin, Minsoo

Noh. Sphingosylphosphorylcholine down-regulates filaggrin gene transcription through NOX5-based NADPH

oxidase and cyclooxygenase-2 in human keratinocytes. Biochem. Pharmacol. Accepted and in press. (as a

corresponding author).

2. Minsoo Noh, Hyeonju Yeo, Jaeyoung Ko, Han Kon Kim, Chang-Hoon Lee. MAP17 is associated with the

T helper cell cytokine induced down-regulation of filaggrin transcription in human keratinocytes. Exp.

Dermatol. 2010, 19: 355-362. (as a corresponding author)

3. Jennifer H. Shin, Dong Wook Shin, and Minsoo Noh. IL-17A inhibits adipocyte differentiation in human

mesenchymal stem cells and regulates pro-inflammatory responses in adipocytes. Biochem. Pharmacol. 2009,

77: 1835-1844. (as a corresponding author)

4. Dong Wook Shin, Su Nam Kim, Sang Min Lee, Woojung Lee, Min Jeong Song, Sun Mi Park, Tae Ryong

Lee, Joo-Hyun Baik, Han Kon Kim, Jeong-Ho Hong, and Minsoo Noh. (-)-Catechin promotes adipocyte

differentiation in human bone marrow mesenchymal stem cells through PPARgamma transactivation.

Biochem. Pharmacol. 2009, 77: 125-133 (as a corresponding author)

Minsoo Noh, Ph.D.Skin Research Institute, Amorepacific Corporation Research Center,

Gyeonggi-do, Korea

CURRICULUM VITAE

- 46 -

Recently, industry has been interested in discovery of novel research targets from the whole

genomic transcriptional profiling studies on human diseases and related experimental models.

Public microarray databases such as the NIH Gene Expression Omnibus (GEO) have provided a

plethora of whole genomic microarray data for human clinical samples. In order to find novel

drug targets, we meta-analyzed the public microarray data for dermatological symptoms like

atopic dermatitis, psoriasis, eczema, and acne, especially exploiting the data whose raw image files

are available. Meta-analyses of public microarray databases are limited by the impossibility to

verify the microarray results by independent measurements using identical or similar clinical

samples. Alternatively, gene expression can be assessed using an appropriate cell culture model,

if the data obtained from cultured cells can be extrapolated to the disease conditions under study.

In this study, we used the differentiation of keratinocytes in culture to evaluate the expression

of the target genes identified in the meta-analysis. Because each dermatological disease has its

unique CD4 positive T helper (Th) cell profile, we postulated that the effects of Th cell cytokines

on NHEK may be useful to the confirmation of meta-analysis results. We confirmed that the

mRNA expression profiles in response to Th1, Th2 and Th17 cell cytokines in NHEK may provide

an alternative approach to validate the candidate genes identified in the meta-analyses of the four

dermatological diseases. When we compared the differentially expressed genes across the four

datasets, seven genes, DSG3, KRT6, MAP17, PLSCR1, RPM2, SOD2, and SPRR2B, were

up-regulated and three genes, CHP2, SCGB1D2, and TSPAN8, were down-regulated in all four

skin lesions. Of candidate genes from the meta-analysis, we found that MAP17 was significantly

up-regulated in response to interferon gamma (IFNgamma, interleukin 4 (IL-4), IL-6, IL-17A, or

IL-22, in NHEK. In an attempt to evaluate whether MAP17 regulates the expression of cornified

envelope-associated genes at the 1q21 locus such as filaggrin, loricrin, and involucrin, we found

that the over-expression of MAP17 in HaCaT keratinocytes significantly decreased the expression

of filaggrin. Taken together, the Th cell cytokine-induced up-regulation of MAP17 expression may

be linked to the down-regulation of filaggrin in NHEK, which may be associated with the abnormal

epidermal differentiation observed in the dermatologic diseases.

Insight mining through meta-analysis of public

microarray databases

Minsoo Noh

AmorePacific Corporation R&D Center

Bench to Clinic

- 49 -

Education

1988-1994 Seoul National University College of Medicine (M.D.): Graduated with honors

(summa cum laude)

2002-2005 Korea University (Ph.D. in microbiology)

Career

1994- 1999 Seoul National University Hospital, Dermatology board

1999- 2002 Chunchon Armed Forces General Hospital, Director of Dermatology

2002-present Leaders Clinic, Director

2005-present Lecturer, Silver-care manager program, Sookmyung Women’s University

2008-present Adjunct Assistant Professor of Dermatology, Seoul National University College of

Medicine

2009-present Editorial Board Member of World Journal of Stem Cell

2009 Marquis Who’s who in the world

Selected Publications

- Kim PM, Park BS, Chapter <Liposuction>, In: Aesthetic Dermatologic Surgery (official publication

of The Korean Society for Aesthetic and Dermatologic Surgery.) Hanmi medical publishing Co.,

2007; 331-345

- Park BS, Kim WS, Chapter <Adipose-derived stem cells and their secretory factors for skin aging>,

In: "Textbook of Aging Skin”, Editors M. A. Farage, K.W. Miller and H. I. Maibach. Springer-Verlag.

2009

Selected Papers

1. The hair growth promoting effects of adipose tissue-derived stem cells. Journal of Dermatological Science

2010 Feb;57(2):134-7. Epub 2009 Dec 5.

2. Hair growth stimulated by conditioned medium of adipose-derived stem cells is enhanced by hypoxia:

evidence of increased growth factor secretion. Biomedical Research 2010;31(1):27-34 (first author)

3. Hypoxia enhanced wound-healing function of adipose-derived stem cells: Increase in stem cell proliferation

and up-regulation of VEGF and bFGF. Wound Repair and Regeneration 2009;17(4):540-7 (corresponding

author)

4. The wound-healing and antioxidant effects of adipose-derived stem cells. Expert Opinion on Biological

Therapy 2009;9:879-87 (corresponding author)

Byung-Soon Park, M.D., Ph.D.Leaders Clinic,

Korea

CURRICULUM VITAE

- 50 -

5. Protective role of adipose-derived stem cells and their soluble factors in photo-aging. Archives of Dermatological

Research 2009;301(5):329-36. Epub 2009 Apr 26 (corresponding author)

6. Antiwrinkle effect of ADSC: Activation of dermal fibroblasts by secretory factors Journal of Dermatological

Science 2009;53:96-102 (corresponding author)

7. Evidence supporting antioxidant action of ADSC: Protection of fibroblasts from oxidative stress. Journal of

Dermatological Science 2008;49:133-42 (corresponding author)

8. Whitening effect of ADSC: A critical role of TGF-beta1. Biol Pharm Bull 2008; 31(4):606-10 (corresponding

author)

9. Adipose-derived stem cells and their secretory factors as a promising therapy for skin aging. Dermatologic

Surgery 2008;34(10):1323-6 (first author)

10. Wound healing effect of Adipose-derived stem cells: A critical role of secretory factors on human dermal

fibroblasts. Journal of Dermatological Science 2007;48:15-24 (corresponding author)

11. Prevention of thyroidectomy scar by the treatments using a New 1550 nm Fractional Erbium-glass laser.

Dermatologic Surgery Dermatol Surg 2009 Aug;35(8):1199-205. Epub 2009 Jan 21.

12. Effect of quilting sutures on hematoma formation after liposuction with dermal curettage for treatment of

axillary hyperhidrosis: A randomized clinical trial. Dermatologic Surgery 2008;34(8):1010-5

13. Novel porous matrix of hyaluronic acid for the three-dimensional culture of chondrocytes. International

Journal of Pharmaceutics 2009;369:114-20

14. Mechanism for increased bioavailability of tacrine in fasted rates. Journal of Pharmacy and Pharmacology

2006;58:643-9

15. Vitamin D receptor polymorphism is associated with psoriasis. Journal of Investigative Dermatology

1999;112:113-116 (first author)

- 51 -

The current topics of increasing interest in the dermatological field are anatomical-functional

damage to the skin and every possible means to counteract the injurious effects. Regenerative

medicine refers to the use of body’s own stem cells and growth factors for repair or restoration.

Adipose-derived stem cells (ADSCs) were shown to increase the survival rate in fat transplantation.

The diverse pharmacologic effects of ADSCs and their secretory factors will be reviewed in this

lecture. To date, clinical application of cultured ADSCs in human skin is in the early stage and

can be related to issues/concerns.

In addition, ADSCs have to overcome the obstacles in that they are difficult both to handle

and to commercialize in an industrial point of view. Therefore, new methods and materials to

overcome these limitations are needed. Secretomes of ADSC have numerous advantages over

cell-based therapies and might have greater potential in skin regeneration. As such, the studies

demonstrated that the photodamage can be reversed by utilizing the ADSCs/their secretory factors

alone or in combination with other devices minimizing unwanted effects. Identification of active

proteins will be the next goal, and drug development using these proteins will suggest better

strategies for skin aging in the future.

From bench to bedside in the application

of stem cells

Byung-Soon Park, M.D., Ph.D.

Leaders Clinic, Korea

FreeCommunication

(FC-1 ~ FC-9)

- 55 -

FC-1

Early-onset sarcoidosis and Blau syndrome: Autoinflammatory

granulomatosis associated with NOD2 mutations causing constitutive

NF-kappaB activationNobuo Kanazawa

Department of Dermatology, Wakayama Medical University, Wakayama, Japan

Once, early-onset sarcoidosis (EOS) was considered as a rare subgroup of sarcoidosis, which was

distinguished from ordinary sarcoidosis by juvenile onset, high incidence of arthritis rather than

lung involvement, and poor prognosis. Now it is evident by recent genetic analyses that sporadic

EOS and familial Blau syndrome (BS) share not only the clinical characteristics of juvenile-onset

systemic granulomatosis mainly affecting skin, joints and eyes, but also the genetic etiology of

gain-of-function NOD2 mutations causing constitutive NF-kappaB activation (Kanazawa et al,

Blood 2005). Subsequent cohort study of genotype-phenotype correlations in 20 Japanese EOS/BS

cases showed that more obvious visual impairment was observed in cases with R334W mutation

compared to the cases with R334Q mutation, correlated with the level of in vitro basal NF-kappaB

activation through these NOD2 mutations (Okafuji et al, Arthritis Rheum 2009). However, the

precise mechanism is still unclear how such NOD2 mutations result in granuloma formation,

although Nod2-mediated intracellular signaling pathway has been intensely investigated.

To address this issue, human monocytic THP-1 cells expressing disease-associated NOD2

mutations were generated and analyzed. Unexpectedly, no significant difference of cytokine

expressions was observed among THP-1 derivatives without stimulation. Then, PMA was added

to induce differentiation of THP-1 cells into macrophage-like cells. Morphologically, THP-1 cells

spread pseudopods and attached to the culture plate for several days after PMA addition, then

again floated in medium to proliferate. Interestingly, mutant THP-1 cells spread more and longer

pseudopods and attached to the culture dish for longer period. By RT-PCR, expression of PDGF-B

was specifically induced in mutant THP-1 cells after short exposure to PMA. Furthermore, by flow

cytometric analysis, although similarly upregulated ICAM-1 expression was observed on both

control and mutant THP-1 cells at short period after PMA addition, following downregulation of

its expression was specifically inhibited in mutant cells. Considering the previously-reported

involvement of PDGF-B and ICAM-1 in ordinary sarcoidosis, these effects should contribute to

the NOD2 mutation-associated granuloma formation.

- 56 -

FC-2

HMG-CoA reductase inhibitors have an inhibitory effect on Th17

cytokines-induced CCL20 expression in keratinocytes in vitro

Taegyun Kim, M.D.2, Dashlkhumbe Byamba, M.D.

2, Jung Hwan Je, Ph.D.

1, Jin Mo Park, M.D.

1,

Hyo Jin Roh, M.D.1, Min-Geol Lee, M.D., Ph.D.

1

1Department of Dermatology and Cutaneous Biology Research Institute, Brain Korea 21 Project for

Medical Science, Yonsei University College of Medicine, Seoul, Korea2These Authors Equally Contributed to this Work

Psoriasis is a common chronic inflammatory cutaneous disorder. Recently a new subset of

helper T cells (Th), Th17 cells, became known to be a crucial pathogenic immune cell type in

psoriasis. Th17 cells display chemokine receptor CCR6, the macrophage inflammatory protein-3α

(MIP-3 /CCL20) receptor; CCR6+ T cells and CCL20 are abundant in psoriatic skin. The majorα

source of CCL20 in psoriatic lesions is epidermal keratinocytes, which can induce CCL20 through

Th17 cytokines. HMG-CoA reductase inhibitors, generically referred to as statins, are lipid-

lowering drugs which have become the core of a popular therapeutic regimen for reducing

cardiovascular morbidity. However, it has become apparent that statins not only lower lipid levels

but also modulate the immune response. In this context, we investigated a possible role for statins

in reducing Th17 cytokines-induced CCL20 expression in keratinocytes in vitro. To measure the

effects of statins on CCL20 expression in HaCaT cells, we used the enzyme-linked immunosorbent

assay. Fluvastatin and simvastatin, but not pravastatin, inhibited CCL20 expression induced by

IL-1 , TNF- , and IL-17A. For functional implications of the inhibitory effect of statins, weβ α

performed the chemotaxis assay and the flow cytometry. Treatment with IL-1 , TNF- , and IL-17Aβ α

increased the number of migrated nonadherent cells from PBMCs; however, it was observed that

fluvastatin and simvastatin significantly inhibit this chemotactic migration. These results indicate

that certain statins could inhibit Th17 cytokines-induced CCL20 expression in HaCaT cells resulting

in reduced migration of immune cells in vitro.

- 57 -

FC-3

Callus is formed by hyperproliferation with incomplete differentiation and

increase of adhesive molecules in the epidermis

Su Hee Kim1, Soo Il Kim

1, Hye In Choi

1, Young Jin Choi

1, Kyung Cheol Sohn

2, Young Lee

2,

Chang Deok Kim2, Jeung Hoon Lee

2, Young Ho Lee

1

Departments of 1Anatomy, 2Dermatology, School of Medicine, Chungnam National University

General features of callused skin are known previously, but the mechanism of callus formation

is not fully understood.

To further elucidate mechanism of callus formation by investigating the genes/proteins expression

related to keratinzaiton and adhesion/desquamation in the callused skin.

The skins of the dorsum of the foot, the center of the plantar arch, and the anterior aspect of

the heel were obtained from the fresh cadavers. H-E and Nile red stains and immunohis-

tochemistry for protease-activated receptor 2 (PAR2), involucrin, filaggrin, and corneodesmosin

(CDSN) were performed in the tissue sections. RT-PCR for the genes related to keratinization and

adhesion/desquamation was performed with the tissue of the three sites.

The stratum corneum in the dorsum of the foot was split in the H-E stained section, but not

split in most of the stratum corneum in the callused skin. Expression of adhesive proteins such

as CDSN, desmoglein 1 (DSG1), and desmocollin 1 (DSC1) was increased in the callused skin

compared with the normal plantar skin. Most of the molecules related to keratinization such as

involucrin, filaggrin, caspase 14, and calcium sensing receptor (CaSR). However, PAR2, involved

in corneocyte formation, expression was incomplete in the stratum corneum in the callused skin.

The number of the proliferating cells in the stratum basale was significantly increased in the

callused skin compared with the normal plantar skin. The cell shape the stratum corneum was

thick, not squamous, in the callused skin.

Our data suggest that callus is formed by hyperproliferation with incomplete differentiation and

increase of adhesive molecules in the epidermis.

- 58 -

FC-4

Expression and functional role of Sox9 in keratinocyte differentiation

Ge Shi1, Zheng jun Li

1, Kyung-Cheol Sohn

1, Dae-Kyoung Choi

1, Young Ho Lee

2, Tae-Jin Yoon

3,

Young Lee1, Chang Deok Kim

1, Jeung-Hoon Lee

1

1Departments of Dermatology, 2Anatomy,School of Medicine, Chungnam National University, Daejeon;3Department of Dermatology, School of Medicine, Gyeongsang National University, Jinju, Korea

Sox9 (SRY (sex determining region Y)-box 9) is an autosomal gene involved in the control of

the male-determining pathway. It has been known that Sox9 is expressed in outer root sheath

of hair follicle and exerts its action as an importance regulator in maintenance of stemness for

hair cells. However, its expression and putative role in epidermal keratinocytes has not been well

elucidated yet. In this study, we examined the expression and functional role of Sox9 in

keratinocyte differentiation. Immunohistochemical staining showed that Sox9 is predominantly

expressed in basal layer. Consistent with this result, Sox9 mRNA level was markedly decreased

by the calcium treatment of cultured keratinocytes. And, Western blot also showed that the protein

level for Sox9 was decreased by calcium in a temporal manner. To investigate its putative role,

we made a recombinant adenovirus harboring the expression cassette for Sox9. Overexpression

of Sox9 prevented calcium-induced loricin and involucrin expression. Consistent with,

overexpression of Sox9 decreased the promoter activities of involucrin and loricrin. In addition,

Sox9 overexpression resulted in significant down-regulation of the cell cycle-related genes p21.

Interestingly, Sox9 expression was highly increased in several skin diseases such as psoriasis, BCC

and SCC. UVB can up-regulated Sox9 expression in cultured skin keratinocytes and Sox9 can

protect against UVB induced cell death. Together, these results suggest that Sox9 is an important

regulator for keratinocyte proliferation and differentiation, and may have related with many of

skin diseases that are characterized by the hyperproliferative potential of keratinocytes.

- 59 -

FC-5

H19 RNA downregulation stimulated melanogenesis in melasma

Yun-Seok Choi1, Nan-Hyung Kim

1, Chang-Hoon Lee

2, Ai-Young Lee

1

1Department of Dermatology, Dongguk University School of Medicine, 2Division of Basic Science, National

Cancer Center, Goyang, Korea

A variety of factors, including ultraviolet (UV) exposure, have been implicated in the pathogenesis

of melasma. However, UV-induced hyperpigmentation usually recovers spontaneously, whereas

melasma does not. Recently, we detected downregulation of the H19 gene on microarray analysis

of hyperpigmented and normally pigmented skin from patients with melasma, and identified

significant clinical correlations. The H19 downregulation was not accompanied by a reciprocal

change of the imprinted gene, IGF2. Moreover, methylation pattern of the H19 promoter region

in maternal ICR was variable. The H19 knockdown in melanocyte monoculture did not result in

obvious tyrosinase overexpression, whereas the knockdown in a mixed cell culture system,

composed of H19 siRNA transfected normal human keratinocytes and non-transfected normal

human melanocytes, did induce not only a tyrosinase overexpression but also an increase of

melanosome transfer. Estrogen treatment of the H19 RNA knockdown in the mixed cell culture

was more than an additive effect on the tyrosinase overexpression, whereas UV irradiation was

not. These findings suggest that downregulation of H19 and a sufficient dose of estrogen might

be involved in the development of melasma.

- 60 -

FC-6

Identification of up-regualted proteins in psoriasis vulgaris using proteomics

Jae-We Cho, Kyu-Suk Lee


Psoriasis is characterized by epidermal proliferation combined with incomplete terminal

differentiation, as well as an inflammatory response responsible for the chronic nature of the

lesions. To investigate the differential protein profiling between lesional and non-lesional skin in

psoriasis, we analyzed the proteome from non-lesional and lesion skin using proteomics. Our data

showed that several proteins involving DNA synthesis or redox system were increased in lesional

skin compared to non-lesional skin; TF (Serotransferrin), Tubulin beta-2C chain, ATP5B, thymidinie

phosphorylase, dihydropyrimidinase-related protein 2, protein disulfide-isomerase A3, aldehyde

dehydrogenase, isoform 1 of 14-3-3 protein sigma, serum amyloid P-component, heat shock protein

beta-1, glutathione S-transferase P, peroxiredoxin-2. Furthermore we confirmed the increased

expressions of isoform 1 of 14-3-3 protein sigma, glutathione S-transferase P, and peroxiredoxin-2,

in lesional skin using Western blot. In conclusion, modulatory proteins for DNA synthesis and

redox system, such as isoform 1 of 14-3-3 protein sigma, glutathione S-transferase P, and

peroxiredoxin-2 play roles in pathogenesis in psoriasis, and we have tried to study the functional

roles of these proteins in psoriasis.

- 61 -

FC-7

MyD88 mediates UV-induced inflammatory responses and cell apoptosis in

mouse skin in vivo

Youngae Lee, Kyung-hwan Kong, Se Rah Lee, Hyun-Sun Yoon, Kyu Han Kim, Jin Ho Chung


Aging Research, Clinical Research Institute, Seoul National University Hospital; Institute of

Dermatological Science, Seoul National University, Seoul, Korea.

Myeloid differentiation factor 88 (MyD88) is known as an adaptor protein for the Toll-like

receptor (TLR) family and participates in signal transduction by binding to the cytoplasmic Toll/

IL-1 receptor (TIR) domains of activated TLR. Our previous study showed that MyD88 regulates

basal- and UV-induced expressions of IL-6 and MMP-1 in the human epidermal keratinocytes. To

investigate the role of MyD88 in UV-induced skin responses in mouse skin in vivo, MyD88

knockout (MyD88 KO) mice and their wild-type (WT) counterparts were irradiated by 200mJ/cm2

of UV. Skin samples were obtained at 48 hrs after UV irradiation. UV-induced expressions of

interleukine-1β (IL-1 ), IL-6, Cox-2 and MMP-13 were significantly increased in WT mice, but wereβ

not changed in MyD88 KO mice. The number of TUNEL-positive cells in the epidermis of MyD88

KO mice after UV irradiation was less than that of WT mice. Expression of cleaved caspase-3 by

UV was also less in MyD88 KO, compared with that in WT mice. However, UV-induced skin

thickness and Ki-67 expression level didn’t show any significant differences between MyD88 KO

mice and WT mice. Taken together, our results show that MyD88 mediates IL-1 , IL-6, Cox-2 andβ

MMP-13 expression, and cell apoptosis by UV irradiation.

- 62 -

FC-8

β-catenin regulates melanocyte dendricity through the modulation of PKCζ

and PKCδ

Jin-Hwa Kim1, Kyung-Cheol Sohn

2, Tae-Young Choi

2, Mi Yoon Kim

2, Hideya Ando

3,4,

Sun Ja Choi5,6, Sooil Kim

7, Young Ho Lee

7, Jeung-Hoon Lee

2, Chang Deok Kim

2, Tae-Jin Yoon

1

1Department of Dermatology and Institute of Health Sciences, School of Medicine, Gyeongsang National

University, Jinju; 2Department of Dermatology and Research Institute for Medical Sciences, School of

Medicine, Chungnam National University, Daejeon, Korea. 3Skin Aging and Photo-aging Research Center,

Doshisha University, Kizugawa, Kyoto; 4Kobe Skin Research Institute, Kobe, Hyogo, Japan. 5Department of

Visual Design, Daeduk University, Daejeon;. 6Department of Advanced Organic Materials Engineering,

Chonbuk National University, Jeonju; 7Department of Anatomy, School of Medicine, Chungnam National

University, Daejeon, Korea.

The Wnt/ -catenin signaling pathway is involved in the melanocyte differentiation andβ

melanoma development. However, the effect of -catenin for dendrite formation has not beenβ

clearly elucidated yet in normal human epidermal melanocytes (NHEM). To investigate the effect

of -catenin, we transduced NHEM with recombinant adenovirus expressing -catenin. Forcedβ β

expression of -catenin led to the dramatic morphological changes of NHEM, including theβ

reduction of dendrite length and enlargement of cell body. Concomitantly with, the protein levels

for dendrite formation-related molecules, such as Rac1 and Cdc42, were markedly decreased. In

addition, phosphorylation of p38 MAPK was significantly reduced by -catenin, potentiating itsβ

inhibitory role for dendrite formation. Interestingly, overexpression of -catenin led to the increaseβ

of PKC level, while PKC was decreased by -catenin, suggesting that those PKCs were -ζ δ β β

catenin-downstream modulators in NHMC. When PKC was overexpressed, dendrites wereζ

shortened, with the reduced protein levels for Rac1 and Cdc42. In contrast, PKC overexpressionδ

led to the elongation of dendrites, with the increased levels for Rac1 and Cdc42. These results

suggest that -catenin play an inhibitory role for dendrite formation through the modulation ofβ

PKC and PKC .ζ δ

Key Words: -catenin, dendrite, normal human epidermal melanocytes, PKC , PKCβ δ ζ

Training Course in

Cutaneous Biology

- 65 -

Education

Mar. 1972-Feb. 1974 Graduated from the Premedical School of Seoul National University

Mar. 1974-Feb. 1978 Graduated from the Medical College of Seoul National University and

received the Degree of M.D.

Mar. 1979-Feb. 1981 Completed a master's course in Dermatology at Medical College of Seoul

National University and received the degree of M.S.

Mar. 1983-Feb. 1989 Completed a Ph.D. course in Microbiology at Medical College of Seoul

National University and received the degree of Ph.D.

May 1993-Aug. 1995 Post-doctoral fellowship in Skin Biology Laboratory, NIAMS, NIH, USA

Employment

Mar. 1978-Feb. 1979 Internship at Seoul National University Hospital

Mar. 1979-Feb. 1983 Residentship at Department of Dermatology, Seoul National University

Hospital

Feb. 1983-Apr. 1986 Military duty as a chief of Department of Dermatology in Pohang Armed

Forces General Hospital

Oct. 1986- Instructor (1986-1988)

Assistant professor (1986-1992)

Associate professor (1992-1998)

Professor (1998-present)

Department of Dermatology, College of Medicine, Chungnam National

University

Personal Membership

1) Korean Society of Dermatology

2) Korean Society of Molecular Biology

3) Korean Society for Investigative Dermatology

4) Society for Investigative Dermatology

5) Korean Society for Psoriasis

Jeung Hoon LeeProfessor, Department of Dermatology, College of Medicine,

Chungnam National University

CURRICULUM VITAE

- 66 -

Career

1) March 2007- March 2009 Chairman of Board of Directors, Korean Society for Investigative

Dermatology

2) Nov 2006- Nov 2008 Director, Research Institute for Medical Science, Chungnam

National University

Major Publications

1. Lee JS, Yoon HK, Sohn KC, Back SJ, Kee SH, Seo YJ, Park JK, Kim CD, Lee JH. Expression of N-terminal

truncated desmoglein 3 (deltaNDg3) in epidermis and its role in keratinocyte differentiation. Exp Mol Med.

2009 Jan 31;41(1):42-50.

2. Yoon HK, Sohn KC, Lee JS, Kim YJ, Bhak J, Yang JM, You KH, Kim CD, Lee JH. Prediction and evaluation

of protein-protein interaction in keratinocyte differentiation. Biochem Biophys Res Commun. 2008 Dec

12;377(2):662-7

3. Kwon YB, Kim CD, Youm JK, Gwak HS, Park BD, Lee SH, Jeon S, Kim BJ, Seo YJ, Park JK, Lee JH. Novel

synthetic ceramide derivatives increase intracellular calcium levels and promote epidermal keratinocyte

differentiation. J Lipid Res. 2007 Sep;48(9):1936-43

4. Choi JM, Ahn MH, Chae WJ, Jung YG, Park JC, Song HM, Kim YE, Shin JA, Park CS, Park JW, Park TK,

Lee JH, Seo BF, Kim KD, Kim ES, Lee DH, Lee SK, Lee SK. Intranasal delivery of the cytoplasmic domain

of CTLA-4 using a novel protein transduction domain prevents allergic inflammation. Nat Med. 2006

May;12(5):574-9.

5. Seo SJ, Ahn JY, Hong CK, Seo EY, Kye KC, Lee WH, Lee SK, Lim JS, Hahn MJ, Kjeldsen L, Borregaard

N, Kim CD, Park JK, Lee JH. Expression of neutrophil gelatinase-associated lipocalin in skin epidermis. J

Invest Dermatol. 2006 Feb;126(2):510-2.

6. Lee WH, Jang S, Lee JS, Lee Y, Seo EY, You KH, Lee SC, Nam KI, Kim JM, Kee SH, Yang JM, Seo YJ,

Park JK, Kim CD, Lee JH. Molecular Cloning and Expression of Human Keratinocyte Proline-Rich Protein

(hKPRP), an Epidermal Marker Isolated from calcium-Induced Differentiating Keratinocytes. J Invest

Dermatol 2005 Nov;125(5):995-1000

7. Seo EY, Namkung JH, Lee KM, Lee WH, Im M, Kee SH, Tae Park G, Yang JM, Seo YJ, Park JK, Deok Kim

C, Lee JH. Analysis of calcium-inducible genes in keratinocytes using suppression subtractive hybridization

and cDNA microarray. Genomics. 2005 Nov;86(5):528-38.

8. Lee JH, Jang SI, Yang JM, Markova NG, Steinert PM. The proximal promoter of the human transglutaminase

3 gene. Stratified squamous epithelial-specific expression in cultured cells is mediated by binding of Sp1 and

ets transcription factors to a proximal promoter element. J Biol Chem. 1996 Feb 23;271(8):4561-8.

- 67 -

The epidermis is the outmost skin layer providing the primary barrier which protects our body

from dehydration, mechanical trauma, and microbial insults. It is a stratified squamous epithelium

in which the major cell type is the epidermal keratinocytes. In this educational lecture, major issues

about epidermal kieartinocytes like those as followed will be briefly discussed.

(1) Keratin intermediate filaments (KIFs). KIFs are elongated a-helix-enriched proteins that are

contained at the range of 30-80% in the epidermis. KIFs are hetero-polymers in epithelial cells.

(2) Development of stratirifed epithelium. During embryogenesis cells of the surface ectoderm

commit to an epidermal fate. After this initial step, keratinocytes undergo a complex and

precisely coordinated program resulting in epidermal stratification with the formation of the

epidermal barrier.

(3) Keratinocyte stem cells. After birth, the epidermis is maintained by the continuous self-renewal

of keratinocyte stem cells. These stem cells give rise to a daughter stem cell and a

transit-amplifying cell, which ultimately undergoes terminal differentiation.

(4) Terminal differentiation of keratinocytes. This transition from proliferating keratinocytes into

the cornified cells is a very complex process requiring the activiation and inactiviation of

a wide variety of genes.

(5) Effects of Ca2 on keratinocyte differentiation. Extracellular calcium concentration is an

important trigger of epidermal differentiation. An increasing gradient of extracellular Ca2+

concentration is present from the basal to the cornified layers. Keratinocytes cultured in vitro

can be induced to be differentiated into a stratified structure when exposed to an increase

in extracelluar Ca2+.

(6) Signal transduction pathways of keratinocyte differentiation. Keratinocyte differentiation

accompanied by activation of many pathways of signal transduction including translocation

of some of the isoforms of PKC to the membrane and increased tyrosine kinase activities.

(7) Epidermal permeability barrier. Barrier function is amply provided by stratum coorneum

organized into 'brick-and-mortar' arrays. These structures represent the keratinocytes of final

differentiation process, which are afforded extra protection via the cornified envelope (CE).

The CE that surrounds individual corneocytes is itself organized into lipid-rich lamellar

bilayer.

Recent progress in skin cell research 1

Keratinocyte

Jeung Hoon Lee

Chungnam National Univ, Korea

- 68 -

Education

1988-1994 M.D. in Medicine, Ajou University School of Medicine

1997-1999 M.S. in Dermatology, Ajou University Graduate School

2001-2003 Ph.D. in Dermatology, Ajou University Graduate School

Professional Experience:

1994-1995 Internship in Ajou University Hospital

1995-1997 Research fellow in Department of Life Science, Pohang University of Science and

Technology, Pohang, Korea

1997-2001 Residency in Department of Dermatology, Ajou University Hospital

2001-2002 Fellowship in Department of Dermatology, Ajou University School of Medicine

2002-2004 Instructor in Department of Dermatology, Ajou University School of Medicine

2004-2008 Assistant Professor in Department of Dermatology, Ajou University School of

Medicine

2008.5-2009.8 Research Professor in Department of Dermatology, University of Nice, France

2008-Present Associate Professor in Department of Dermatology, Ajou University School of

Medicine

Hee Young Kang, M.D., Ph.D.Department of Dermatology, Ajou University School of Medicine,

Suwon, Korea

CURRICULUM VITAE

- 69 -

New tools for melanocyte research

There are recent advances in devices for investigating melanocyte and melanin pigmentation.

Recently a non-invasive imaging tool, in vivo reflectance confocal microscopy (RCM), was introduced

to the dermatology field. The usefulness of RCM in investigating benign pigmentary disorders

including melasma and vitiligo as well as melanocytic tumors was suggested (Kang et al., 2009).

A new technique for evaluating melanosome transfer from melanocytes to keratinocytes in vitro

was introduced (Ando et al, 2009). This method seems simple and allows the spectrophotometric

visualization of melanosome uptake by keratinocytes in vitro.

Molecular pathway of tanning

The tumor suppressor protein p53 is thought to promote tanning by stimulating the transcription

of a melanogenic cytokine, POMC in keratinocytes. Yang et al. (2008) showed that UV irradiation

represses TGF-beta in keratinocytes, and repression of TGF-beta upregulates PAX3 in melanocytes,

which is associated with UV-induced pigmentation. The TGF-beta-PAX3 signaling pathway interacts

with the p53-POMC/MSH-MC1R signaling pathway. Murase et al. (2009) further supported the

essential role of p53 in hyperpigmentary spots via the regulation of paracrine-cytokine signaling.

The upregulated transcription factors (MITF, SOX9, SOX10, and PAX3) during UV exposure in vivo

were shown in a recent study from Hearing’s group (2010). As a skin cancer prevention strategy,

Abdel-Malek et al. (2009) reported the use of short MSH-related peptides that can stimulate the

MC1R receptor.

Wnt signaling in skin pigmentation

MITF is a master regulator of pigmentation and is a target for Wnt pathway. Cho et al. (2009)

found that cardamonin inhibited pigmentation through suppression of Wnt/beta-catenin signaling.

DKK1, an inhibitor of Wnt signaling secreted by fibroblasts, not only affects melanocytes and

suppresses their proliferation and differentiation, but it also decreases melanin transfer from


Recent knowledge in melanocyte research

Hee Young Kang

Department of Dermatology, Ajou University School of Medicine, Suwon, Korea

- 70 -

melanocytes to keratinocytes through the suppression of PAR-2, explaning why palmoplantar

epidermis is hypopigmented (Yamaguchi et al., 2008, 2009).

Regulators controlling melanogenesis

The synthesis of melanin pigments is regulated by a variety of signal transduction pathway.

Recently, it was reported that p38 regulates pigmentation via ubiquitin-proteasomal degradation of

tyrosinase (2010). A new enzyme which regulates melanin synthesis, NADPH:quinone oxidoreductase-

1 (NQO1), was identified. Choi et al. (2009) reported that NQO1 increases melanin synthesis,

probably via the suppression of tyrosinase degradation.

Lipid, skin barrier and pigmentation

UV irradiation affects the epidermal barrier function. Gunathilake et al. (2009) explored the

possibility that stress to the epidermal barrier influenced the development of pigmentation in

humans. The role of lipid-mediated signaling in melanocyte function was shown suggesting

therapeutic application of lipid-based therapies in pigmentary disorders (Saha et al., 2009).

Ectopic synthesis of melanin in human body and non-pigmentary roles of melanocytes

Melanocytes are mainly found in the skin of the human body. Recent studies suggested that

melanin seem to be everywhere in the body including visceral adipose tissue and the heart

(Randhawa et al., 2009; Levin et al., 2009). A growing body of evidence also suggested that

melanocytes may have non-pigmentary roles including immunomodulation. (Ye et al, 2009; Kang

et al., 2009).

References

Kang et al., Reflectance confocal microscopy for pigmentary disorders.Exp Dermatol. 2009 Nov 2. Ando et al.,

Keratinocytes in culture accumulate phagocytosed melanosomes in the perinuclear area. Pigment Cell

Melanoma Res 2010;23(1):129-33

Yang et al., Inhibition of PAX3 by TGF-beta modulates melanocyte viability. Mol Cell 2008;32(4):554-63.

Murase et al., The essential role of p53 in hyperpigmentation of the skin via regulation of paracrine melanogenic

cytokine receptor signaling. J Biol Chem 2009;284(7):4343-53.

Choi et al., Regulation of human skin pigmentation in situ by repetitive UV exposure: molecular characterization

of responses to UVA and/or UVB. J Invest Dermatol 2010

Abdel-Malek et al., alpha-MSH tripeptide analogs activate the melanocortin 1 receptor and reduce UV-induced

DNA damage in human melanocytes.Pigment Cell Melanoma Res 2009;22(5):635-44.

Cho et al., Cardamonin suppresses melanogenesis by inhibition of Wnt/beta-catenin signaling. Biochem Biophys

Res Commun 2009;390(3):500-5.

Yamaguchi et al., Regulation of skin pigmentation and thickness by Dickkopf 1 (DKK1). J Invest Dermatol Symp

Proc 2009;14(1):73-5.

Yamaguchi et al., Dickkopf 1 (DKK1) regulates skin pigmentation and thickness by affecting Wnt/beta-catenin

signaling in keratinocytes. FASEB J 2008;22(4):1009-20.

- 71 -

Bellei et al., P38 regulates pigmentation via proteasomal degradation of tyrosinase. J Biol Chem 2010 Jan 6.

Choi et al., Impact of NAD(P)H:Quinone Oxidoreductase-1 on Pigmentation. J Invest Dermatol 2009 Sep 17.

Gunathilake et al., pH-regulated mechanisms account for pigment-type differences in epidermal barrier function.

J Invest Dermatol 2009;129(7):1719-29.

Saha et al., Sphingolipid-mediated restoration of Mitf expression and repigmentation in vivo in a mouse model

of hair graying. Pigment Cell Melanoma Res 2009;22(2):205-18.

Randhawa et al., Evidence for the ectopic synthesis of melanin in human adipose tissue. FASEB J 2009;23(3):835-43

Levin et al., Melanocyte-like cells in the heart and pulmonary veins contribute to atrial arrhythmia triggers. J Clin

Invest 2009;119(11):3420-36.

Yu et al., Cultured human melanocytes express functional toll-like receptors 2-4, 7 and 9. J Dermatol Sci 2009;56(2):

113-20.

Kang et al., Imiquimod, a Toll-like receptor 7 agonist, inhibits melanogenesis and proliferation of human melanocytes.

J Invest Dermatol 2009;129(1):243-6.

- 72 -

학 력

1974-1980 연세의대 의학과 학사

1981-1983 연세대학교 대학원 의학과 석사

1983-1986 연세대학교 대학원 의학과 박사

경 력

1980. 3-1981. 2 연세의료원 인턴

1981. 3-1984. 2 연세의대 피부과학교실 레지던트

1985. 5-1985. 7 서독 함부르크 연구원Institute of Hygiene

1991. 9-1993. 8 미국 의 피부과NCI 및(NIH) Special Volunteer Visiting Associate

(topic: skin immunology about Langerhans cell and gamma delta T cell)

1984. 6- 연세의대 피부과학교실 연구원 전임강사 조교수 부교수 교수, , , ,

2005. 3- 연세의료원 의료선교센터 소장

현 재

연세의대 피부과학교실 교수 연세의료원 의료선교센터 소장 몽골 연세친선병원 이사장1. , , ,

전주예수병원 이사

2. 대한의학협회 대한피부과학회 대한피부연구학회 대한천식 및 알레르기학회 대한면역학회, , , , , Society

of Investigative Dermatology 정회원(USA)

편집위원 대한피부과학회지3. : Experimental Dermatology(Europe),

대한피부과학회 피부연구학회 전 상임이사 현 이사5. , ,

대한수지상세포연구회 전 회장 현 이사6. ,

피부암연구회 전 회장7.

Min-Geol LeeDepartment of Dermatology, Yonsei University College of Medicine,

Seoul, Korea

CURRICULUM VITAE

- 73 -

피부의 수지상세포는 여러 아형의 세포들로 구성되어 있으며 피부에서 병원체와 같은 외부의 위험,

신호를 인지하고 이에 대한 방어기전으로 와 를 시작하는데 있어innate immunity adaptive immunity

파수꾼 같은 핵심적인 기능을 한다 피부 수지상세포. 에는 표피의 랑(Cutaneous dendritic cells, DC)

게르한스세포 와 진피의 수지상세포(Lagnerhans cells, LC) (interstitial/dermal dendritic cells, DDC)

로 크게 나눌 수 있으며 그 외, IDEC 과 수지상(Inflammatory dendritic epidermal cells) plasmacytoid

세포 가 있다(plasmacytoid DC) .

최근 암 자가면역질환 장기 이식분야 등에서 수지상세포의 역할에 대한 많은 연구들이 진행되고, ,

있는데 수지상세포에 관한 많은 이해들이 바로 랑게르한스세포의 연구를 통하여 시작되었다 피부과, .

역에서는 알레르기성 접촉 피부염에서 이 세포에 관한 역할이 잘 알려져 있고 최근 아토피피부염,

에서의 역할에 대한 보고들이 많다 그리고 감염성 질환뿐 아니라 피부암에서의 수지상 세포의 역할.

등에 관한 많은 연구들이 진행되고 있으며 최근 환자의 수지상세포를 이용한 면역치료에 대한 보고,

들도 많다.

최근에는 표피의 수지상세포인 랑게르한스세포는 이때까지 생각해 왔던 면역 자극에 관여하기 보

다는 면역관용 에 주로 관여하고 오히려 진피 수지상세포가 면역 자극(immune tolerance) , (immune

에 관여하리라는 보고들이 많다 랑게르한스세포와 진피 수지상세포를 위주로 피부의stimulation) .

수지상세포에 대하여 나누려 한다


Langerhans cell and dermal dendritic cells

Min-Geol Lee

Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea

- 74 -

Education

1978.03-1984.02 Seoul National University College of Medicine, Seoul, Korea (M.D.)

1986.03-1988.02 Graduate School, Seoul National University, Seoul, Korea (M.S.)

1991.03-1993.08 Graduate School, Seoul National University, Seoul, Korea (Ph.D.)

Professional Experience

1985.03-1988.02 Resident, Department of Dermatology, Seoul National University, Hospital, Seoul,

Korea

1988.03-1991.04 A staff doctor, Department of Dermatology, Capital Armed Forces General

Hospital, Seoul, Korea

1991.05-1993.02 Research Fellowship, Department of Dermatology, Seoul National University

College of Medicine, Seoul, Korea

1997.03-1999.02 Research Fellow, Department of Dermatology, University of Michigan, USA

1993.03-Present Instructor, Assistant Prof., Research Fellow, Associate Prof.,

Professor, Department of Dermatology, Seoul National University College of

Medicine, Seoul, Korea

2004.08-2006.07 Associate Dean of Research Affairs, Seoul National University, Seoul, Korea

2004.08-2006.07 Associate Head of Industry-Academic Cooperation Foundation, Seoul National

University, Seoul, Korea

2005.05-2006.08 President, Seoul National University Industry Foundation, Seoul National

University, Seoul, Korea

2007.11-Present Fellow, Medical Sciences Division, The Korean Academy of Science and

Technology, Seoul, Korea

Award

1992, 1995, 2001 - Donga Academic prize in The Korean Dermatological Association

2003 - Young Investigator’s prize in Seoul National University Hospital

2003 - In-Bong Academic prize in The Korean Dermatological Association

2003 - A Special jury prize for Reserch paper in European Academy Dermatology &

Venereology

2005- SCI I.F prize in Seoul National University Hospital, Seoul National University College of

Medicine Dean

Jin Ho Chung, M.D., Ph.D.Professor, Department of Dermatology, Seoul National University Hospital, Seoul, Korea

CURRICULUM VITAE

- 75 -

2009- Shim Ho-Seob prize in Seoul National University Hospital, Seoul National University

College of Medicine Dean

Sepciality and Research Field of Interest

Photobiology, Photomedicine

Skin aging and photoaging

Autoimmune skin diseases

- 76 -

The dermis is fibrous, filamentous, diffuse, and cellular connective tissue elements that contains

many components, including nerve and vessels, and many cells including fibroblasts and

macrophages. Fibroblast is the regular resident of the dermis and is a mesenchymally derived cell.

Fibroblast is responsible for the synthesis and degradation of connective tissue matrix proteins

and a number of soluble factors. The connective tissue matrix of the dermis is comprised primarily

of collagenous and elastic fibers, proteoglycans and glycosaminoglycans. Fibroblasts produces

these connective tissue components and provide a structural extracellular matrix framework.

Fibroblast also promote interaction between epidermis and dermis by synthesis of soluble

mediators. In this lecture, the roles and functions of fibroblasts will be discussed.

Recent progress in ECM 4

ECM production by fibroblasts

Jin Ho Chung, M.D, Ph.D

Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea

- 77 -

학 력

1988-1995 학사 성균관대학교 유전공학과,

1995-1997 석사 한국과학기술원 생명과학과,

1997-2001 박사 한국과학기술원 생명과학과,

경 력

1997-2001 삼성생명과학연구소

분자바이러스실험실

Research Fellow

2001-2002 삼성생명과학연구소

인간유전체 연구사업단

Post-Doctoral Fellow

2002-2007 NIH, National Cancer Institute

Laboratory of Cancer Biology and Genetics

Post-Doctoral Fellow

현재2007- 가천의과학대학교 이길여암당뇨연구원

종양세포생물학 실험실

조교수

논 문

Suntaek Hong, Ho-Jae Lee, Seong Jin Kim, Ki-Baik Hahm. Connection between inflammation and carcinogenesis

in Gastrointestinal tract; abnormal TGF- signaling and their corrections for chemoprevention. World Jβ

Gastroenterology. 2010 Accepted.

Lee YS, Kim JH, Kim ST, Kwon JY, Hong S, Kim SJ, Park SH. Smad7 and Smad6 bind to discrete regions

of Pellino-1 via their MH2 domains to mediate TGF-beta1-induced negative regulation of IL-1R/TLR

signaling. Biochem Biophys Res Commun. 2010 In Press.

Yoon Jae Kim, Suntaek Hong. Cancer prevention through regulation of TGF- signaling-related inflammatoryβ

processes. Cancer Prev Res. 2009;14(4):283-291.

Han SU, Kwak TH, Her KH, Cho YH, Choi C, Lee HJ, Hong S, Park YS, Kim YS, Kim TA, Kim SJ. CEACAM5

and CEACAM6 are major target genes for Smad3-mediated TGF-beta signaling. Oncogene. 2008 Jan

24;27(5):675-83.

Suntaek Hong, Chan Lee, Seong-Jin Kim. Smad7 Sensitizes Tumor Necrosis Factor Induced Apoptosis through

the Inhibition of Antiapoptotic Gene Expression by Suppressing Activation of the Nuclear Factor-{kappa}B

Suntaek Hong, Ph.D.Professor, Department of Dermatology, College of Medicine,

Chungnam National University

CURRICULUM VITAE

- 78 -

Pathway. Cancer Research. 2007 Oct 1;67(19):9577-83.

Suntaek Hong, Lim S, Li AG, Lee C, Lee YS, Lee EK, Park SH, Wang XJ, Kim SJ. Smad7 binds to the adaptors

TAB2 and TAB3 to block recruitment of the kinase TAK1 to the adaptor TRAF2. Nature Immunol. 2007

May;8(5):504-13.

Choi KC, Lee YS, Lim S, Choi HK, Lee CH, Lee EK, Hong S, Kim IH, Kim SJ, Park SH. Smad6 negatively

regulates interleukin 1-receptor-Toll-like receptor signaling through direct interaction with the adaptor

Pellino-1. Nature Immunol. 2006 Oct;7(10):1057-65.

Kim BG, Li C, Qiao W, Mamura M, Kasperczak B, Anver M, Wolfraim L, Hong S, Mushinski E, Potter M,

Kim SJ, Fu XY, Deng C, Letterio JJ. Smad4 signalling in T cells is required for suppression of gastrointestinal

cancer. Nature. 2006 Jun 22;441(7096):1015-9.

Kim BC, Choi JW, Hong HY, Lee SA, Hong S, Park EH, Kim SJ, Lim CJ. Heme oxygenase-1 mediates the

anti-inflammatory effect of mushroom Phellinus linteus in LPS-stimulated RAW264.7 macrophages. J

Ethnopharmacol. 2006 Jul 19;106(3):364-71.

Lim HW, Hong S, Jin W, Lim S, Kim SJ, Kang HJ, Park EH, Ahn K, Lim CJ. Up-regulation of defense enzymes

is responsible for low reactive oxygen species in malignant prostate cancer cells. Exp Mol Med. 2005 Oct

31;37(5):497-506.

- 79 -

The extracellular matrix (ECM) and ECM proteins plays a key role in organ formation and tissue

homeostasis. Also, the ECM is important in phenomena as diverse as stem cell niches, cancer and

genetic diseases. ECM proteins typically include multiple, independently folded domains whose

sequences and arrangement are highly conserved. Some of these domains bind adhesion receptors

such as integrins that mediate cell-matrix adhesion and also transduce signals into cells. However,

ECM proteins also bind soluble growth factors and regulate their distribution, activation and

presentation to cells. There are increasing evidences for specific and direct binding of growth

factors to ECM proteins. Both fibronectin and vitronectin bind hepatocyte growth factor and form

complexes of Met and integrins, leading to enhanced cell migration. Drosophila collagen IV binds

Dpp and enhances its interactions with BMP receptors. The regulation of TGF-beta signaling by

ECM proteins is one of the well known examples of these interactions. Each of the precursors

of TGF-beta is cleaved by a furin protease to the mature TGF-beta and its propeptide, known

as latency-associated peptide. These latent complexes bind to ECM proteins and enhance the

effective activation of TGF-beta. On the other hand, TGF-beta regulates the expression of ECM

proteins in the wound healing and other biological processes. In this session, I will present the

relationships of growth factor signaling, especially TGF-beta signaling, with ECM and the roles

in pathological conditions.


Cross-talk between ECM and TGF-beta signaling

Suntaek Hong

Laboratory of Cancer Cell Biology, Lee Gil Ya Cancer and Diabetes Institute,

Gachon University of Medicine and Science

- 80 -

학력 경력/

1984. 2 연세의대 졸업

1988. 2 피부과전문의 취득

1991. 5 - 1994. 2 연세의대 피부과학교실 강사

1994. 3 - 1996. 2 미국 의대 피부 및 피부생물학과Thomas Jefferson Postdoctoral Fellow

1996. 3 - 2002. 2 연세의대 피부과학교실 조교수

1999. 4 - 2000. 6 미국 의대 피부외과 임상연수 피부 및 피부생물학과Thomas Jefferson /

방문교수

2002. 3 - 2007. 2 연세의대 피부과학교실 부교수

현재2007. 3 - 연세의대 피부과학교실 교수

현재1988. 02 - 대한피부과학회 정회원

현재1992. 03 - 대한피부연구학회 정회원

현재2000. 07 - 대한미용피부외과학회 정회원

현재2000. 11 - 미국피부외과학회 정회원

현재2001. 07 - 미국피부연구학회 정회원

1999. 11 - 2001. 10 대한피부과학회 학술위원회 간사

2003. 11 - 2005. 10 대한피부과학회 학술위원회 간사

2001. 03 - 2003. 02 대한미용피부외과학회 학술이사

2003. 03 - 2005. 02 대한미용피부외과학회 간행이사

2004. 12 - 2006. 11 대한미용피부외과학회 감사

현재2005. 03 - 대한피부연구학회 간행이사

2006. 12 - 2008. 11 대한미용피부외과학회 총무이사

현재2008. 12 - 대한미용피부외과학회 감사

현재2009. 03 - 대한피부암학회 총무이사

Kee Yang ChungDepartment of Dermatology, Yonsei University College of Medicine,

Seoul, Korea

CURRICULUM VITAE

- 81 -

피부에 존재하는 세포외기질 은 광학현미경 상 교원질섬유(extracellular matrix) (collagen fiber),

망상섬유 탄력섬유(reticular fiber), 로 나뉜다 교원질은 동물에서 가장 함유량이 많은(elastic fiber) .

단백질이고 교원질 섬유가 구조를 이루고 있다 교원질섬유는triple helix . 1~20 두께의 구불구불mμ

한 모양을 보이고 이 섬유는, 30~100 두께의 교원질nm 소섬유 로 구성되어 있다 교원(collagen fibril) .

질소섬유는 64~67 길이의 의 모양을 보인다 망상섬유는 으로 염색nm D-banding . silver impregnation

했을 때 검게 보이는 미세한 섬유의 망으로 관찰되며 근세포 지방세포 세포 등의 표면을, , Schwann

덮는다 망상섬유는 전자현미경 상 개개의 교원질소섬유 또는 그의 작은 다발. 약 로 이루어져( 30 mn)

있고 교원질섬유와 연결되어 있다 탄력섬유는 등의 미세소섬유, . fibrillin 와 의 구(microfibril) elastin

성 비율에 따라서 로 이루어져 있고 은oxytalan-elaunin-elastic fiber elastin 0.1~0.2 두께의m elastinμ

소섬유로 구성되어 있다 따라서 세포외 기질은 형태학적으로 조직과 세포를 받쳐주는 구조물의 역할.

을 하는 교원질섬유들과 조직에 가해지는 힘을 균등하게 분배해서 조직의 탄성을 유지하게 해 주는

미세소섬유 탄력섬유들로 구성되어 있다- .


Collagen, elastin, and reticular fibers

Kee Yang Chung

Yonsei University College of Medicine, Seoul, Korea

Oral Posters(PO-1 ~ PO-6)

- 85 -

PO-1

Activators of Peroxisome Proliferator-Activated Receptor alpha (PPARα)protect UV-induced changes of MMP-1 and procollagen via catalase

induction in human skin fibroblasts

Mi Hee Shin, Hyun-Sun Yoon, Dong Hun Lee, Jang-Hee Oh, Eunyoung Seo, Jin Ho Chung


Aging Research, Clinical Research Institute, Seoul National University Hospital, and Institute of

Dermatological Science, Medical Research Center, Seoul National University, Seoul, Korea

We have reported that among the antioxidant enzymes, the activity of catalase decreased

significantly in the dermis of photoaged and aged skin. Therefore, we suggested that the induction

of catalase expression may offer a good strategy for the treatment and prevention of aging and

photoaging in human skin. Peroxisome proliferator-activated receptor alpha (PPAR ) is a nuclearα

receptor involved in transcriptional regulation of lipid metabolism, fatty acid oxidation, and

glucose homeostasis. In addition, PPAR activation stimulates the expression of antioxidantα

enzymes such as catalase. In this study, we examined whether PPAR activator modulates theα

expression of MMP-1 and procollagen through catalase regulation in human skin fibroblasts. We

found that PPAR and catalase mRNA levels were significantly decreased by UV irradiation andα

in the aged skin fibroblasts. Treatment with PPAR agonists, bezafibrate and Wy14643, increasedα

protein, mRNA and activity of catalase in dermal fibroblasts. PPAR activators, bezafibrate andα

Wy14643, inhibited the UV-induced MMP-1 expression and recovered the UV-induced decrease

of procollagen expression. Also, in aged dermal fibroblasts, Wy14643 decreased the expression of

MMP-1 and increased the levels of procollagen and catalase. Furthermore, UV-induced ROS was

decreased by PPAR activator, Wy14643. These results suggest that up-regulated catalase by PPARα

activation might scavenge the UV-induced ROS. Transfection with PPAR siRNA decreasedα α

catalase level and abolished all beneficial effects of Wy14643 in dermal firboblasts. In summary,

our data indicate that PPAR activator increases the antioxidant enzyme catalase, leading toα

scavenging ROS, and protects the skin from UV irradiation as well as intrinsic skin aging process.

Therefore, we propose that the PPAR activator would be a good candidate to prevent and treatα

skin aging.

- 86 -

PO-2

The study of regulatory mechanism of IL-17 induced Egr-1 expression in

HaCaT human keratinocytes

Jae Eun Choi1,2, Sang Hoon Jeong

1, Yoon-Hee Park

1, Sang Min Lee

2, Jae Hwan Kim

2,

Il Hwan Kim2, Sang Wook Son

1,2, Young Chul Kye

1,2

1Laboratory of Cell Signaling and Nanomedicine, 2Department of Dermatology and Division of Brain Korea

21 Project for Biomedical Science, Korea University College of Medicine, Seoul, Korea

Interleukin (IL)-17 has been reported to play an important role in the pathogenesis of diverse

immune-mediated diseases, including psoriasis, rheumatoid arthritis, asthma and atopic dermatitis.

The early growth response (Egr)-1 is a transcription factor which plays an important role in the

regulation of cell growth, differentiation, survival, apoptosis and immune responses. Emerging

evidences demonstrate that transcription of the Egr-1 gene is up-regulated in the psoriatic skin

lesions, implicating that Egr-1 function as a regulator in the pathogenesis of psoriasis. However,

the molecular mechanism underlying the induction of Egr-1 expression in psoriasis has not been

clarified. In this study, we explored the regulatory mechanism of Egr-1 induction by IL-17 in HaCaT

keratinocytes. The results show that IL-17 induces Egr-1 expression in a dose- and time-dependent

manner in HaCaT human keratinocytes. We also found that IL-17 induces nuclear translocation

and promoter activity of Egr-1. Inhibition of the extracellular signal-regulated kinase (ERK)

mitogen-activated protein kinase (MAPK) signals, but not c-Jun N-terminal kinase (JNK) or p38,

strongly attenuated IL-17 induced Egr-1 expression in HaCaT keratinocytes. Our findings suggest

a novel signaling mechanism by which IL-17 can trigger the induction of Egr-1 transcription via

activation of the ERK MAPK signaling cascades in human keratinocytes. Thus Egr-1 might be one

of the important genetic factors involved in the cross-talk of signals between immune cells and

epidermal keratinocytes in inflammatory skin diseases such as psoriasis.

- 87 -

PO-3

Filaggrin knockdown enhanced the production of IL-6, IL-8, and thymic

stromal lymphopoietin from HaCaT cells via TLR stimulation

Kyung Ho Lee1, Kyung-Ah Cho

2, Ji-Yoon Kim

2, Ji Hye Baek

1, So-Youn Woo

2, Jin-Woo Kim

1

1Department of Dermatology, College of Medicine, The Catholic University of Korea,2Departments of Microbiology, School of Medicine, Ewha Womans University, Seoul, Korea

The skin acts as an indispensible barrier to protect various invaders from the outside. The

epidermis provide physical and chemical defense of innate immunity. The disturbed skin barrier

allows entering innocuous antigens into the skin followed by triggering immune responses and

initiate inflammation. Filaggrin (filament-aggregating protein) aggregates the keratin filaments into

tight bundles leading to collapse of the coneocytes into flattened shape. Filaggrin deficiency or

aberrant expression result the phenotype of ichthyosis vulagaris and atopic dermatitis, characterized

by a disturbed skin barrier and dry skin. Filaggrin-deficient mice showed the predisposition of

skin inflammation and sensitization of irritants and haptens through epidermis. As keratinocytes

are first barrier against exogenous antigens and they possess Toll-like receptors (TLRs) as pattern

recognition molecules to activate antimicrobial innate immune response. To determine whether the

level of filaggrin expression affected the TLR-mediated responses of keratinocytes, we transfected

filaggrin siRNA into human keratinocyte cell line, HaCaT, and measured the IL-1 , IL-6 and IL-8β

secretion. We found that TLR stimulation did not enhance the IL-1 but IL-6 secretion wasβ

increased by poly (I : C). In addition, IL-8 secretion was increased under Pam3CSK4 stimulus in

filaggrin knockdown cells. In addition, expression of TSLP is increased in poly (I : C) treated

filaggrin knockdown layer. Therefore, these results suggest that the decreased level of filaggrin

may trigger innate immune response via TLR stimuli and contribute to pathogenesis of inflammatory

skin disease.

- 88 -

PO-4

HnRNP-A2/B1 as a Target Antigen of Anti-Endothelial Cell IgA Antibody in

Behçet’s Disease

Sung Bin Cho, M.D., Keun Jae Ahn, Ph.D., Suhyun Cho, M.D., Shin-Wook Kang, M.D., Ph.D.,

Ju Hee Lee, M.D., Ph.D., Yong-Beom Park, M.D., Ph.D., Kwang Hoon Lee, M.D., Ph.D.,

Dongsik Bang, M.D., Ph.D.


Medicine, Seoul, Korea (S.B.C., K.J.A., S.H.C., J.H.L., K.H.L., D.B.), Division of Nephrology, Department

of Internal Medicine, BK21 Project for Medical Science, Yonsei University College of Medicine, Seoul,

Korea (S-.W.K.). Division of Rheumatology, Department of Internal Medicine, Institute for Immunology

and Immunologic Diseases, BK21 Project for Medical Science, Yonsei University College of Medicine,

Seoul, Korea (Y-.B.P.).

Streptococcus sanguis, Viridans group streptococci, has been proved its major role in immuno-

pathogenesis of Behçet’s disease (BD) which mainly inhabit the mucous membrane of the mouth,

throat, colon, and female genital tract. Because IgA presents in large quantity at mucosal sites

and is responsible for mucosal immunity, the aim of our study was to identify the anti- endothelial

cell IgA antibody-binding human dermal microvascular endothelial cell (HDMEC) antigen.

We detected a target protein by using Western blotting and immunoprecipitation, and then

searched for a similar protein after the amino acids were sequenced by nanoflow liquid

chromatography/electrospray ionization/tandem mass spectrometry (LS-EOI-MS-MS) analysis. We

next searched for the DNA sequence of the target protein at the National Center for Biotechnology

Information (NCBI) and purified the recombinant target protein by gene cloning. We then

investigated the reactivities of the recombinant target protein in BD.

We performed Western blotting of extracts of HDMECs with selected serum samples of seven

BD patients and A 36-kD protein band was detected in all seven patients. The 36-kD protein band

obtained from immunoprecipitation was excised and analyzed by nanoflow LS-EOI-MS-MS and

a peptide fingerprint was obtained. Using the NCBI scanning algorithm, we found that the protein

band showed the amino acid sequences of hnRNP-A2/B1. Reactivity to hnRNP-A2/B1 was

detected in 35 of 44 BD patients (79.5%) on Western blots, whereas none of 20 healthy controls

and 13 IgA nephropathy patients presented reactivity against hnRNP-A2/B1.

The hnRNP-A2/B1 protein is the target protein of serum anti-endothelial cell IgA antibody in

BD patients. This is the first report of the presence of IgA antibodies to hnRNP-A2/B1 in

endothelial cells from the serum of BD patients.

- 89 -

PO-5

Cyclosporine stimulates the expression of CDK4 through NFATc1

suppression: A good candidate for therapeutic modality in alopecia areata

Chae-Young Lee, Young-Hun Kim, Ki-Ho Kim

Department of Dermatology, Dong-A University College of Medicine

The hair follicles grow in a cyclic pattern through various stages and this hair growth is

spontaneously activated from the quiescent bulge stem cells or activated from precocious anagen

by NFATc1 inhibitors such as cyclosporine and FK506. G1/S phase specific CDK4 is repressed

by NFATc1 at transcriptional level in resting state (telogen phase). Upon the spontaneous activation

of hair growth or its activation induced by NFATc1 inhibitors, NFATc1 expression is lost and

CDK4 repression is relieved along with the inhibited BMP signaling in hair follicle.

Alopecia areata (AA) is believed to be an autoimmune disease in which T lymphocytes infiltrate

in peribulbar and intrabulbar patterns and the miniaturized hair follicles increase and then round

shaped sparse hairy or hairless patches develop. Differently from the known action mechanism

of cyclosporine as an immunosuppressant against activated T cell, this drug can work as a potent

inducer for hair growth in physiologic and pathologic conditions.

In this study, we planned to investigate the hair growing property of cyclosporine in vitro

conditions. Briefly, human hair follicles were separated from the scalp of AA patients (n=6) and

cultured in William’s E medium with cyclosporine (200, 500, 1000, 2000 nM) and drug-free controls;

First, we performed the hair follicle cultures during 5~20 days and observed the changes in

histomorphologic patterns to determine the optimal culture condition. Second, we studied NFATc1

expression to find out the changes of its expression from quiescence to activation by cyclosporine.

Last, we examined the topographic expression of CDK4 and its changes according to various

concentrations of cyclosporine treatment.

The results are followed: First, the hair follicle cultures well survived in 9 or 10 days by the

appearance in histomorphologic pattern. Second, NFATc1 was expressed in considerable amount

at presumably bulge stem cell area in the cyclosporine-free culture, and downregulated with

increasing concentration of cyclosporine. Third, CDK4 expression was upregulated judging from

the extended topographic appearance from the bulge stem cells to the hair bulb matrix cells and

ORS (outer root sheath) keratinocytes with increasing concentration.

Taken together, theses findings indicate cyclosporine induces CDK4 expression by the NFATc1

suppression, which relieve the repressed CDK4 as a precocious activation from quiescence in the

bulge of hair follicle. And in vitro hair follicle culture is an useful tool to predict the hair growing

properties by beneficial agents in physiologic and pathologic conditions like AA, especially

considering the related signaling events in calcineurin-NFAT pathway.

- 90 -

PO-6

A decline of TRPV6 function derives from a decrease of vitamin D activation

and accounts for disturbed epidermal calcium gradient followed by skin

barrier alteration in aged skin

Minyoung Jung1, Yoonhee Lee

1, Byung-Il Yeh

2, Seung Hun Lee

3, Eung Ho Choi

1

1Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju;2Department of Biochemistry, Yonsei University Wonju College of Medicine, Wonju;3Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea

Epidermal Ca++regulates keratinocyte differentiation and plays an important role in forming

skin barrier. Because epidermal Ca++gradient is restored with the recovery of skin barrier after

its disruption, a disturbance in the recovery of Ca++gradient delays skin barrier recovery. TRPV6

as a calcium ion channel, belonging to the superfamily of transient receptor potential channels

constitutes an apical Ca++ entry mechanism in active Ca++ transport in the intestine, which has

been also found in the epidermis of mammalian skin recently. TRPV6 modulates an influx of Ca++

into keratinocyte, and its expression is directly up-regulated by 1 , 25 dihydroxyvitamin D3. Facialα

skin of aged humans showed the loss of epidermal Ca++ gradient, and the synthesis of cutaneous

vitamin D3 was declined with aging. We hypothesized that this disrupted epidermal Ca++ gradient

is caused by a decrease of TRPV6 function due to decreased vitamin D activation with aging.

The mRNA expression of TRPV6 and vitamin D receptor (VDR) on fully aged skin (87 weeks

old hairless mice) decreased; moreover their mRNA expression was not enough increased after

3-day low-dose (50 mJ/day) UVB irradiation compared to young skin. Western blot for TRPV6 and

VDR protein expression showed very similar results with mRNA. Topical ketoconazole, an

inhibitor of 1 , 25 dihydroxyvitamin D3, decreased TRPV6 expression even after UVB irradiationα

under immunohistochemical stain.

In conclusion, a decline of TRPV6 function could be derived from decreased vitamin D activation

and accounts for disturbed epidermal Ca++ gradient and altered skin barrier in aged skin.

Key word: Calcium ion channel, TRPV6, Vitamin D receptor, Aged skin

Posters(P-1 ~ P-45)

- 93 -

P-1

Modification of transcription factors with O-linked N-acetylglucosamine

during the process of keratinocyte differentiation

Eun jin Lee, Kyung-Cheol Sohn, Sang-Shin Lee, Jeung-Hoon Lee

Department of Dermatology, School of Medicine, Chungnam National University

In eukaryotes, many of proteins are posttranslationally modified to achieve their proper func-

tionality. These include proteolytic cleavage, acetylation, methylation, prenylation, phosphorylation

and glycosylation. The modification of proteins with O-linked N-acetylglucosamine (O-GlcNAc) is

recently discovered protein modification, which is performed by O-linked GlcNAc transferase

(OGT) in nucleocytoplasm. O-GlcNAcylation is occurred in serine and threonine residues by

O-linkage of GlcNAc as a monosaccharide form, and not elongated into more complex structure.

Terminal differentiation of skin keratinocytes is a vertically directed multi-step process that is

tightly controlled by the sequential expression of a variety of genes. Besides, various regulatory

proteins are activated and/or repressed by posttranslational modifications, although the total levels

for these proteins are not changed. In this study, I attempted to investigate whether the new

posttranslational modification, O-GlcNAcylation, may affect keratinocyte differentiation. To this

end, I performed Western blot analysis with anti-GlcNAc antibody against total proteins prepared

after calcium treatment of keratinocytes. Overall pattern of O-GlcNAcylation was decreased,

however, some of proteins were highly O-GlcNAcylated during the calcium-induced keratinocyte

differentiation. These results suggest that O-GlcNAcylation is authentic posttranslational modifica-

tion, which affects the keratinocyte differentiation. To confirm this notion, I perfomed immuno-

histochemistry analysis against OGT, a key enzyme to catalyze the O-GlcNAcylation to target

proteins. Interestingly, expression of OGT was increased in upper granular layer of epidermis.

Concomitantly, the expression of OGT was increased in calcium-induced keratinocyte differentia-

tion in vitro. These results suggest that O-GlcNAcylation of target proteins may have impact for

the expression of differentiation markers. Next, to find the target for O-GlcNAcylation, I focused

on several transcription factors involved in keratincoyte differentiation. Interestingly, transcription

factors including SP1 were O-GlcNAcylated by OGT overexpression. Together, these results

suggest that increase of OGT in calcium-induced differentiation may affect the activities of several

transcription factors, thereby promoting the keratinocyte differentiation.

- 94 -

P-2

EC-SOD transgenic mice show thin epidermis by apoptosis through

galectin-7 and COX-2 expression

Joon-seok Lee, Yunsang Lee, and Tae-Yoon Kim


The Catholic University of Korea

Extracellular superoxide dismutase (EC-SOD) is an anti-oxidant enzyme, which is located in the

extracellular matrix of tissues, and plays an important role in terms of preventing many disease

caused by oxidative stress. However, other functions of EC-SOD are not well known, so we

generated EC-SOD transgenic mice to investigate the functions of EC-SOD. We found that the

epidermis in EC-SOD transgenic mice was thinner than that of wild type mice. In addition, we

demonstrated that the thin epidermis of EC-SOD transgenic mice results from the apoptosis of

epidermal cells by TUNEL assay. To elucidate which molecules are involved in the EC-SOD-induced

apoptosis, we performed two-dimensional electrophoresis; the results showed that the epidermis

of EC-SOD transgenic mice produces more galectin-7, which is known to be a pro-apoptotic factor,

than that of the wild type. Furthermore, we showed that transfection of EC-SOD expressing

plasmids induces production of galectin-7 and galectin-7 expressing plasmids induce pro-apoptotic

proteins in keratinocyte cell lines, HaCaT cells, suggesting that EC-SOD induces apoptosis through

increased galectin-7 expression. Finally, we demonstrated that EC-SOD-induced expression of

galectin-7 results from the production of COX-2. Taken together, our results indicate that over-

expression of EC-SOD could induce apoptosis through COX-2 and galectin-7 in the epidermis.

These results imply that EC-SOD plays a role as not only an ROS scavenger but also as a pro-

apoptotic factor via COX-2/galectin-7 pathways in epidermis.

- 95 -

P-3

Assessment of phototoxicity and skin irritation potential of nanopolystyrene

and nanoTiO2 using cultured keratinocytes, a human skin equivalent model

and an in vivo model

Yoon-Hee Park2, Sang Hoon Jeong

2, Sang Min Yi

1, Jae Hwan Kim

1, Jae Eun Choi

1,

Byeong Hyeok Choi2, Meyoung-Kon Kim

3, Il-Hwan Kim

1, Sang Wook Son

1

1Department of Dermatology and Division of Brain Korea 21 Project for Biomedical Science, Korea

University College of Medicine, Seoul; 2Laboratory of Cell Signaling and Nanomedicine, Korea University

College of Medicine, Seoul; 3Department of Biochemistry & Molecular Biology, Korea University College of

Medicine, Seoul, Korea

Nanoparticles increasingly used in many ways in pharmaceutical and commercial products

including sunscreen. But, little literature is available on its skin toxicity and irritation potential.

We have investigated the toxicity of nanoparticles of polystyrene, and titanium dioxide in human

keratinocytes cell line, a human skin equivalent model (HSEM), and animal model.

Nanoparticles were morphologically characterized by transmission electron microscopy. We

evaluated the cytotoxic effects of nanoparticles on cultured HaCaT keratinocytes. Phototoxicity tests

were carried out on 3T3 fibroblast cells, 3D EpiDermTM models, and Hartley albino guinea pig

skin. In addition, we also evaluated the irritation potentials of nanoparticles on 3D EpiDermTM

models and rabbit skin.

Polystyrene nanoparticles reduced the cell viability of HaCaT cells in dose-dependent manner.

These nanoparticles were classified as non-phototoxicity in the 3T3 NRU phototoxicity. These data

correspond well with those from the HSEM, and animal model. 3D EpiDermTM models revealed

no irritation. Furthermore, this result concurred with Draize skin irritation test.

The present study indicates that nanoparticles of polystyrene and titanium dioxide don’t cause

phototoxicity and acute cutaneous irritation. Furthermore, our findings suggest that the described

HSEM offers a more accurate means than conventional culture-based systems for determining the

relative toxicities of NPs.

- 96 -

P-4

Our new devised method determining the intial dose of narrow-band UVB

treatment with colorimetric L* value

Jai Il Youn, In Ho Kwon, Hyuck Hoon Kwon

Department of Dermatology, Seoul National University College of Medicine

The initial doses of narrow-band UVB (NBUVB) treatment for psoriasis were usually 50~70%

of minimal erythema dose (MED). However, the determination of MED needs the additional time

of 24 hour for checking, which could lead to the discomfortablity for patient. The dermatologist

might determine the MED subjectively by the gross examination of perceptible erythema.

Therefore, the determination of MED needs the doctor’s technical experience. It was demonstrated

that colorimetric L* value might be useful for predicting the sensitivity to NBUVB irradiation

owing to the correlation between the MED and the colorimetric L* value.

The aim of the present study is to compare two methods determining the initial dose by MED

50% and colorimetric L* value in NBUVB phototherapy with respect to efficacy and safety for

Korean psoriasis patients with skin phototype III to V.

The retrospective study was performed for 39 psoriasis patients who received NBUVB

phototherapy three times weekly by a 20% dose incremental regimen at Seoul National University

Hospital between January 2007 and March 2009. Twenty and 19 patients was treated with the

initial dose determined by the MED 50% and colorimetric L* value, respectively. We evaluated

the L* value with the Minolta Spectrophotometer CM-2002 (Minolta, Tokyo, Japan). Accordingly,

the initial doses of NBUVB were 500 mJ, 400 mJ, and 300 mJ in the cases of L* < 62, 62 L*

66 and 66 < L*, respectively.

The MED and colorimetric method acheieved Gr IV in 11 of 20 patients (55.0%) and 12 of 19

patients (63.2%), respectively (p=0.605). The adverse effects such as erythema and itching are 12

of 20 patients (60.0%) and 8 of 19 patients (42.1%) in two methods (p=0.264). Moreover, no

statistically significant difference between two treamtment group was found with respect to the

number of sessions, duration of treatment, final dose, and cumulative dose.

We suggest that our new devised method determining the intial dose of NBUVB with

colorimetric L* value could substitute or replace the MED checking methods with respect to

efficacy and safety.

- 97 -

P-5

Effect of light emitting diodes (LED) on melanoblast cell line-A potential

treatment modality for vitiligo

Sumathy Babitha1, Jeong-Hyun Shin

2, SunA Yoon

3, Sang-Joo Park

3, Eun-Ki Kim

3

1BK21 Center for Advanced Medical Education, Inha University School of Medicine, Incheon;2Department of Dermatology, Inha University School of Medicine, Incheon;3Department of Biological Engineering, Inha University, Incheon, Korea

Vitiligo is an acquired disorder of pigmentation in which depigmentation of skin and hair occur

due to loss of melanocytes from the epidermis. It is known that the existence of inactive melanoblasts

in the hair follicles provide a melanocytes resource for repigmentation in vitiligo. Migration of

these melanoblasts from the outer root sheath of hair follicles into clinically depigmented epidermis

is crucial for the repigmentation in vitiligo therapy.

Low-power lasers and light-emitting diodes (LED) are well-accepted therapeutic tools in the

treatment of infected, ischemic, and hypoxic wounds, along with other soft tissue injuries. LED

has been reported to stimulate proliferation, and migration of various types of cells, including

fibroblasts, endothelial cells, and keratinocytes. Migration of stem cells from hair follicle to

epidermis is one of the processes of wound healing. Therefore, we hypothesized that LED can

stimulate melanoblast to migrate and thus it may be an effective treatment modality for vitiligo.

There are few reports describing LED treatment for vitiligo in the literature, however, the

mechanism of LED on melanoblasts is not known. To evaluate the potential of LED on melanoblast,

Melb-a cell line was subjected to LED irradiation and its effect on differentiation, proliferation and

migration of melanoblasts were investigated. MSH was used as positive control, because it isα

well known ultraviolet light-derived melanoblast stimulating factor. In result, LED stimulated

migration of Melb-a cells but differentiation. MSH stimulated both migration and differentiationα

of melb-a cells. The findings of the present study would be significant in understanding the

mechanism of LED treatment for vitiligo.

- 98 -

P-6

Genetic polymorphisms of HLA-F and HLA-G are associated with

susceptibility to non-segmental vitiligo in Korean populations

Lee EJ1, Shin MK

1, Hong MS

2, Uhm YK,

2Lee MH

1

Kohwang Medical Research Institute and Departments of 1Clinical Pharmacology and 2Dermatology, School

of Medicine, Kyung Hee University, Seoul, Korea

Vitiligo, a commonly acquired hypopigmented disorder, has shown strong evidence for a genetic

factor in the pathogenesis by many epidemiologic studies about familial aggregations, and human

leukocyte antigens (HLA) associations. It has been associated with different HLA in different ethnic

groups.

We have investigated polymorphisms association between HLA-F and HLA-G gene and non-

segmental vitiligo (NSV) in Korean population.

The ten SNPs in the HLA-F and eight SNPs in the HLA-G genotypes assay on Affymetrix

Targeted Genotyping Chip in 231 vitiligo patients and 382 controls. We used SNPStats, Haploview,

Hapanalyzer, and SNPAnalyzer programs for the evaluation of genetic data. The multiple logistic

regression models were analysis of HLA-F and HLA-G genetic distribution of polymorphisms. We

conducted direct sequencing of the significant three SNPs in HLA-G gene.

The five SNPs (rs9258170, rs3998799, rs2235383, rs1736922, and rs3734814) in the HLA-F gene

and rs2735022, rs1736936, and rs1632933 in the HLA-G gene showed strong linkage disequilibrium.

The rs2735022, rs1736936 and rs1632933 was significant association with NSV in the recessive

models (rs2735022 and rs1736936; p < 0.04; OR, 1.53; 95% CI, 1.01-2.34, rs1632933; p < 0.05; OR, 1.52;

95% CI, 1.00-2.32), respectively.

These results suggest that the three SNPs in HLA-G gene may be associated with the

susceptibility of NSV in Korean population.

- 99 -

P-7

MKK6 increases the melanocyte dendricity through the regulation of Rho

family GTPases

Mi Yoon Kim1, Jin-Hwa Kim

1, Tae-Young Choi

1, Yu Jin Kim

1, Young Lee

1, Young Ho Lee

2,

Chang Deok Kim1, Jeung-Hoon Lee1, Tae-Jin Yoon3

Department of 1Dermatology, 2Anatomy, School of Medicine, Chungnam National University, Daejeon;3Department of Dermatology, School of Medicine, Gyeongsang National University, Jinju, Korea

Dendrite formation requires actin polymerization, and Rho family GTPases including RhoA,

Rac1 and Cdc42 are well implicated in this process. It has been documented that RhoA regulates

the formation of the actin stress fibers though bundling of pre-existing filaments, whereas Rac1

and Cdc42 are required for the formation of lamellipodia and filopodia, respectively, via de novo

actin polymerization. In other systems, Rac1 and Cdc42 are shown to be related with the p38

MAPK pathway. To investigate the involvement of p38 MAPK in melanocyte dendrite formation,

we made the recombinant adenovirus expressing MKK6, an upstream MAPKK for p38 MAPK.

Interestingly, the activation of p38 MAPK by overexpression of MKK6 resulted in increase of

dendrite number in normal human melanocytes cultured in vitro. When MKK6 was overexpressed

in melanoma cell line SK-mel-24, dendrite length was dramatically increased. To examine whether

the activation of p38 MAPK by MKK6 expression affects the Rho family GTPases, we perfomed

Western blot analysis against RhoA, Cdc42 and Rac1. As expected, overexpression of MKK6 led

to the upregulation of Cdc42 and Rac1, while RhoA was slightly decreased by MKK6 overexpression.

These results suggest that activation of p38 MAPK pathway by MKK6 is an important step to

regulate Rho family GTPases, thereby influencing the dendricity of melanocytes.

- 100 -

P-8

Detection of Autoantigen of Melanocyte Reacting with Autoantibodies in Sera

of Vitiligo Patients by Proteomics

Ji Young Kim, Jeong Eun Do, Keun Jae Ahn, Sang Ho Oh

Department of Dermatology, Yonsei University College of Medicine

Vitiligo is an acquired idiopathic hypomelanotic disorder characterized by circumscribed

depigmented macules resulting from the loss of cutaneous melanocytes. Although the exact cause

of vitiligo remains obscure, autoimmunity may play a role in the development of the disease. The

present study was undertaken to find out autoantigens in the melanocytes that reacts with

autoantibody in the sera of vitiligo patients through proteomics and 2 dimentional -Western

blotting.

We collected sera of 22 active vitiligo patients and 14 normal controls, The existence of IgM

autoantibody against proteins of cultured melanocytes was verified through ELISA method. After

sorting out sera with higher values in ELISA, we performed 2-dimensional immunoblotting assay

to detect the site of the protein spot reacting with pooled serum in vitiligo patients against cultured

melanocyte protein. Subsequently, the protein was identified using matrix-assisted laser desorption/

ionization-time of flight mass spectrometry (MALDI-TOF MS) by separating the same site in the

electrophoresis gel.

In the IgM ELISA for melanocyte antigen, the mean (± SD) OD of sera from vitiligo (n=22) was

0.77 (± 0.85) and normal control subjects (n=14) was 0.53 (± 0.32). When values higher than 1.17 (the

mean for normal control + 2 times the SD) were considered positive, five of 22 vitiligo patients

(22.7%) had positive result for IgM. Through MALDI-TOF MS analysis, sera from patients with

vitiligo yielded multiple spots, and the purified proteins were identified as: heat shock protein

70, crystal structure of phosphorylation-mimicking mutant T356d Of Annexin Vi, aminopeptidase

B, glucose-6-phosphate dehydrogenase, fibrin beta, S-adenosylhomocysteine hydrolase, actin-related

protein 1, NADP-dependent isocitrate dehydrogenase, elongation factor Tu, enoyl coA hydratase,

and zinc finger protein 623 isoform 1.

From this preliminary data, we will perform ELISA and Western blotting using recombination

of identified autoantigens to evaluate the rate of existence of antigen-specific antibody in sera of

vitiligo patients. The detection of specific autoantigen reacting with autoantibody in vitiligo will

be helpful for understanding autoimmune pathogenesis of vitiligo and offer a powerful tool for

identifying novel serum markers that may display clinical usefulness in the progression of vitiligo.

- 101 -

P-9

Adipose-derived stem cell-cultured media improves oxazolone induced

atopic dermatitis skin lesions

Haejin Lee, Minyoung Jung, Eung Ho Choi

Department of Dermatology, Yonsei University Wonju College of Medicine

Adipose-derived stem cell-cultured media improves oxazolone induced atopic dermatitis skin

lesions

Stem cells are undifferentiated cells which have the potentials of self-renewal and differentiation.

Adipose-derived stem cell (ADSC) has relative advantages in the accessibility and abundance

compared to other kinds of stem cells and produces many kinds of growth factors and hormones

not determined yet. Therefore, we investigated whether the cultured media of ADSC could be

used as a novel therapeutic material for atopic dermatitis (AD), a representative inflammatory skin

disease. ADSC cultured media was applied topically, twice daily for 5days on oxazolone induced

AD hairless mice model. Topical administration of ADSC cultured media improved the visible

AD lesions through an improving mechanism of epidermal permeability barrier and differentiation

compared to control of fibroblast cultured media. ADSC cultured media increased the LB number

and the expression of anti-microbial peptides (CRAMP, mBD3). Our result implicated that topical

ADSC cultured media would be useful in atopic dermatitis.

- 102 -

P-10

Inhibitory Effects of Effective Microoganism Fermentation Substance (Em-S)

on the Development Atopic Dermatitis-Like Skin Lesions in NC/Nga MICE

Seon Il Jang*, Ji Ye Mok, Kwang-Hyun Park, Na-Na Seong, Ji-Min Park, Jung-Keun Cho, Ji-Won

Choi, and Byung-Eun Moon

Jeonju University Atopy & Health Research Institute, Jeonju, Korea, School of Alternative Medicine &

Health Science, College of Alternative Medicine, Jeonju University, Jeonju, Korea. Department of

Biochemistry, Chonbuk National University Medical School, Jeonju, Korea, Evermiracle research institute,

Jeonju, Korea

In previous study, we have shown that the effective microorganism fermentation substance

(EM-S) by fermentation of medicinal plants with effective microorganisms have an anti-inflam-

matory effects on atopic dermatitis-like lesions in NC/Nga mice. To find new anti-inflammatory

products for skin inflammatory disease such as AD and contact dermatitis, we screened the effects

of EM-S on the development of atopic dermatitis-like skin lesions in NC/Nga Mice. The efficacy

of EM-S was judged by measurement of skin severity, itching behavior, filaggrin, T-cell subset

and CCL10 expressions in ear tissue Topically applied EM-S significantly reduced skin severity

score and itching behavior in NC/Nga mice by the house dust mite antigen (Dermatophagoides

farinse extract, Df) sensitization. In addition, CD4+, CTACK/CCL27 and CCL10 expressions were

significantly reduced by EM-S. Futhermore, EM-S treatment increased the level of the reduced

filaggrin expression by Df sensitization. These results demonstrate that topical application of EM-S

may be an effective substance for the management of AD patients.

- 103 -

P-11

S100A9 correlates with clinical improvement of atopic dermatitis with

immunotherapy

Chang Ook Park1, Ji Yeon Noh

2, Sang Ho Oh

2, Byung Gi Bae

2, Sung Min Noh

2,

Kwang Hoon Lee2

1Department of Dermatology, The Armed Forces Byukjae Hospital, 2Department of Dermatology &


Fifteen patients with moderate to severe atopic dermatitis (AD) undergoing subcutaneous immu-

notherapy (SCIT) with HDM allergens (Alavac ; Bencard, Brenford, UK) for more than 1 year were

recruited to analyze serum before and after SCIT. The serum was analyzed to search for new

protein biomarkers using two-dimensional difference in-gel electrophoresis (2D-DIGE) followed by

mass spectrometry (MS) and nano liquid chromatography (LC)-MS/MS. By comparing pooled AD

serum after SCIT with matched AD serum before SCIT in a pairwise manner, we identified 22

up-regulated and 57 down-regulated spots with intensity changes greater than 2-fold (Student's

t-test, p < 0.05). Among the identified 23 distinct proteins, we focused on S100A9 due to its gene

expression in patients with AD and epidermal expression in other skin diseases. The levels of this

novel protein, identified by both MS and LC-MS/MS, were significantly lower (by 17.66-fold) in

AD serum after SCIT than before SCIT. The eczema area and severity index (EASI) scores in AD

patients decreased significantly after undergoing SCIT (the mean EASI score (± SD), 21.7 ± 9.6

before and 5.6 ± 4.6 after, p < 0.0001). Serum S100A9 levels decreased significantly from 2.5 ± 1.8

ng/mL to 1.7 ± 1.7 ng/mL after immunotherapy (p < 0.005) in parallel with the reduction in EASI

scores. However, three patients had a slight increase in S100A9 levels. We suggest that S100A9

could be a novel immunologic marker for estimating the therapeutic effect of immunotherapy and

monitoring disease activity in patients with AD.

Key Words: Atopic dermatitis, S100A9, S100, immunotherapy, allergy

- 104 -

P-12

Thymic stromal lymphopoietin enhances Th2 cytokine production by

invariant natural killer T cells

Chang Ook Park1, Byung Gi Bae

2, Wen Hao Wu

2, Sang Ho Oh

2, Sung Min Noh

2, Ji Yeon Noh

2,

Keun Jae An2, Kwang Hoon Lee

2

1Department of Dermatology, The Armed Forces Byukjae Hospital; 2Department of Dermatology &


Thymic stromal lymphopoietin (TSLP) is an epithelial cell-derived cytokine produced by human

keratinocytes in AD. TSLP exerts its biological activities by binding to a heterodimeric receptor

consisting of the IL-7 receptor -chainα (IL-7R ) and the TSLP receptor chainα (TSLPR). TSLP not

only triggers adaptive allergic immune responses by stimulating myeloid DCs to induce TH2 cell

responses, but also rapidly induces an innate type of allergic immune response by activating mast

cells and natural killer T (NKT) cells. NKT cells represent a subpopulation of thymus-derived T

cells that co-express a T-cell receptor (TCR) along with typical surface receptors for natural killer

cells. More than 80% of NKT cells express invariant TCR chain V 24-J 18 paired with V 11 inα α α β

humans (or V 14-J 18 paired with V 8, V 7, or V 2 in mice) and are referred to as invariant NKTα α β β β

(iNKT) cells. iNKT cells uniquely recognize glycolipid antigens presented by the nonpolymorphic

MHC class I-like molecule CD1d. A glycolipid isolated from a marine sponge, -galactosylceramideα

( -GalCer), binds CD1d and activates mouse and human iNKT cells. iNKT cells rapidly produceα

large quantities of cytokines, including IL-4 and IFN- , as a manifestation of innate-like immunity.γ

We investigated whether iNKT cells expressed TSLP receptor, and whether these cells were

activated by TSLP. We demonstrated that both TSLP receptor protein and mRNA were expressed

on the surface of iNKT cells. IL-4 and IL-13, but not IFN- , expression increased in theγ

TSLP-treated iNKT cells, although -GalCer-treated iNKT cells expressed high levels of IL-4, IL-13,α

and IFN- . These results suggest that TSLP might directly activate iNKT cells into a TH2 patternγ

in allergic inflammation.

Key Words: Thymic stromal lymphopoietin, invariant natural killer T cells, NKT cells, atopic

dermatitis

- 105 -

P-13

The effect of relaxation therapy on atopic dermatitis

Byung Gi Bae1, Sang Ho Oh1, Chang Ook Park2, Il Ho Park3, Ji Yeon Noh1, Kwang Hoon Lee1

1Department of Dermatology & Cutaneous Biology Institute, Yonsei University College of Medicine, Seoul;2Department of Dermatology, The Armed Forces Byukjae Hospital; 3Department of Psychiatry, Myongji

Hospital, Kwandong University College of Medicine, Gyeonggi, Korea

Both children and adults with atopic dermatitis (AD) have been reported to exhibit abnormalities

of psychological profiles including anxiety, depression, emotional excitability, and inactivity. As

clinical evidence was accumulated, the importance of employing a psychological approach in AD

management has increased. Psychological interventions and programs were reported to be more

effective than conventional treatments alone in terms of severity of eczema, subjective severity,

and effect on quality of life. However, the effects of psychological interventions have been not

evaluated in terms of neuro-immune mediators, such as neurotrophin and neuropeptide. We

assessed the effect of relaxation therapy in terms of atopic dermatitis symptoms, degree of stress,

and neuro-immune mediators.

Twenty-six patients (15 men, 11 women; mean age 23.2 years, range 12-40), with a confirmed

diagnosis of AD according to the criteria of Hanifin and Rajka and a severity of eczema of at

least 15 points according to the eczema area and severity index (EASI), were enrolled in this study.

All subjects did not have previous systemic immunosuppressant agent in a month. The subjects

were randomly divided into two groups. One group was treated with relaxation therapy in

addition to topical treatments and anti-histamines while the other group was treated only with

topical treatments and anti-histamines. Jacobson relaxation therapy, which has been reported to

be effective in panic disorder and generalized anxiety disorder, were carried out as psychological

intervention. In the both groups, before treatments and one month after the treatments, we

evaluated the AD symptoms (EASI score, degree of pruritus, and degree of sleep disturbance),

degree of stress (state-trait anxiety index), and neuro-immune mediators. Among neuro-immune

mediators, we evaluated serum level of nerve growth factor (NGF) and neuropeptide Y (NPY)

using ELISA, both of which have been reported to be strongly associated with anxiety and be

related to aggravation of AD after psychological stress.

Key Words: Atopic dermatitis, Stress, Relaxation therapy, Neuro-immune mediator

- 106 -

P-14

Beneficial effects of the conditioned medium of adipose tissue-derived stem

cells on human follicular cells

Chong-Hyun Won1, Seung-Hyun Shin

1, Gyeong-Hun Park

1, Sung-Eun Chang

1, Mi-Woo Lee

1,

Jee-Ho Choi1, Kee-Chan Moon1, Jee-Soo An2, Oh-Sang Kwon2, Hyeon-Gyeong Yoo2,

Soon-Jin Choi2, Kyu-Han Kim

2

1Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul;2Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea

Adipose tissue-derived stem cells (ADSCs) produce many kinds of growth factors including

insulin-like growth factor binding protein precursors, vascular endothelial growth factor,

hepatocyte growth factor, platelet-derived growth factor and keratinocyte growth factor. These

factors are well-documented to be related to hair growth stimulation. Previously, we reported

ADSCs could promote hair growth in vitro.

To investigate the paracrine effect of ADSCs on human dermal papilla cells (hDPCs) and outer

root sheath cells (hORSCs)

We determined the proliferation of hDPCs and hORSCs after treatment of the conditioned

medium of ADSCs (ADSC-CM) using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide

(MTT) assay. The role of wnt-beta catenin signal pathway and alkaline phosphatase expression

in hDPCs were investigated after ADSC-CM treatment using immunocytochemistry. We examined

the ADSC-CM induced abrogation of hDPC growth suppression by hydrogen peroxide and

dihydrotestosterone.

ADSC-CM treatment significantly enhanced proliferation of hDPCs at concentrations of 25% and

50%, however did not consistently increased that of hORSCs. Nuclear translocation of beta catenin

and the expression of alkaline phosphatase were not affected by ADSC-CM treatment. Pretreatment

with 25% and 50% ADSC-CM for 24 hours abrogated the growth suppression induced by 50 and

100 nM dihydrotestosterone (DHT), and significantly increased hDPC proliferation (p < 0.001). Same

pretreatment in case of 250 and 500 M hydrogen peroxide also increased the hDPC proliferationμ

(p < 0.001).

ADSC-CM promotes hDPC proliferation and recovers the suppression induced by DHT and

hydrogen peroxide. These results indicate ADSC-CM can be beneficial for the growth and

protection against cytotoxic injury by androgen and reactive oxygen species in hDPCs.

- 107 -

P-15

Changes of integral hair lipid according to intrinsic hair aging

Youn-hee Lee1, Youn-Duk Kim1,2, Sung-hae Kim1, Tae-sik Park3, Won-Soo Lee1


College of Medicine, Wonju; 2Central Research Laboratories of Aekyung industrial Co. Ltd., Daejeon;3Laboratory of Lipid Biology, Lee Gil Ya Cancer and Diabetes Institute, Korea

Internal lipids are composed of ceramides, cholesterol, free fatty acid, cholesterol sulfate, fatty

alcohol and phytosphingosine. In this study, we investigated the differences of internal hair lipids

contents between ages.

Human scalp hairs without any chemical treatments such as having hair permanently waved

and bleached were obtained from Asian black haired subjects and used for experiments. We

obtained 3 person samples each age groups. To analysis of lipids contents, we used HPTLC,

LC-Mass.

There were no statistically significant difference of overall lipid contents between age groups.

But the contents of ceramide and sphingosine which are the trace elements of hair lipids were

different. Ceramides contents of forties and fifties are reduced than in young generation, but

Sphingosine which is a precursor of ceramide was not reduced.

We thought these difference of lipids contents might be related the aging of hair.

- 108 -

P-16

Hair growth regulation by the extract of Chrysanthemum Zawadskii

Long-Quan Pi1, Kunhoae Kim2, Jeong-hwan Lee2, Gyeong-Yup Chi2, Xing-Hai Jin1, Yoon-Hee Lee1,

Jae-Hong Ji1, Youn-Duk Kim

1, In-Sik Cho

2, Won-Soo Lee

1



This study was undertaken to investigate the effects of Chrysanthemum zawadskii extract on

hair growth in vivo and in vitro. Chrysanthemum zawadskii extract was applied topically onto

the back of C57BL/6 mice every day for 40 days. Hair shaft elongation was measured by organ

culture model of human scalp hair follicles. Proliferation of human dermal papilla (DP) cells was

determined by MTT assay. mRNA expression level of growth factors related to the hair growth

was determined by reverse transcription polymerase chain reaction. As results, Chrysanthemum

zawadskii extract induce the earlier conversion of telogen to anagen in vivo, promote proliferation

of human DP cells in vitro. In addition, Chrysanthemum zawadskii extract up-regulate VEGF

mRNA expression in cultured human DP cells. These results suggest that Chrysanthemum zawadskii

extract have hair growth promoting potential through the regulation of growth factors in DP cell

and promotion of DP cell proliferation.

- 109 -

P-17

The changes of hair lipid composition after UV irradiation on three ethnic

hairs

Jae Hong Ji1, Youn-Duk Kim

1,2, Sung-Hae Kim

1, Won-Soo Lee

1



Integral hair lipid plays a key role in the maintenance of hair integrity including hydrophobicity

and stiffness. UV irradiation induce photochemical degradation of hair shaft.

The purpose of this study was to investigate lipid changes after UV irradiation in three ethnic

hairs. We had irradiated hair shaft using UV irradiator. We evaluated the changes of hair lipid

using HPTLC, weighing balance and LC-Mass.

The lipid composition of three normal ethnic hairs were similar, but Asian hair has higher

amount of free fatty acid than other two ethnic hairs. Especially African hair has higher amount

of squalene than others. After UV irradiation, 18-MEA level was changed. These pattern was

shown in all three ethnic hairs.

We thought from our results that UV irradiation caused hair weaken, so extractable lipid was

extracted easily. Integral hair lipid has differences between races, and UV irradiation alters the

integral hair lipid.

- 110 -

P-18

The effects of Ornithine Decarboxylase on human hair growth in vitro

Long-Quan Pi1, Xing-Hai Jin1, Jae-Hong Ji1, Yoon-Hee Lee1, Youn-Duk Kim1,

Sungjoo Tommy Hwang2, Won-Soo Lee

1


College of Medicine, Wonju; 2Dr. Hwang’s Hair-Hair clinic, Seoul, Korea

The purpose of the current study was to investigate the expression and effects of ornithine

decarboxylase (ODC) in human hair follicles. We examined the expression of ODC in human hair

follicles and its expression change in organ cultured human hair follicles. Furthermore, we

examined the effects of ODC on follicular keratinocyte (FKC) growth and proliferation/apoptosis-

related molecular expression using -difluoromethylornithineα (DFMO), an irreversible inhibitor of

ODC and small interfering RNA (siRNA) technique. Human hair follicles expressed ODC at mRNA

and protein levels. ODC immunoreactivity can be detected in the epithelium of human anagen

hair follicles. During the transformation from anagen to catagen, ODC expression appeared to be

down-regulated. DFMO inhibited the proliferation of FKC dose-dependently. The levels of P-Erk,

P-Akt, and Bcl-2 decreased while Bax increased after treatment of DFMO. Gene transfection of

ODC siRNA markedly down-regulated the expression of ODC, resulting in the suppression of FKC

proliferation. Moreover, DFMO significantly inhibited human hair growth and promoted apoptosis

in organ cultured human follicles. Altogether, these results indicate that ODC might be an

important regulatory enzyme for human hair growth and hair cycle change.

- 111 -

P-19

Epigallocatechin-3-gallate has an anti-inflammatory effect by regulating

macrophage migration inhibitory factor-induced T helper related chemokines

and cytokines in human HaCaT cells

Sun Up Noh, Hei Sung Kim, Hoon Kang, Jun Young Lee, Hyung Ok Kim, Young Min Park

Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea

Epigallocatechin-3-gallate (EGCG) is well known with its anti-inflammatory effects on chronic

inflammatory skin conditions such as atopic dermatitis (AD). In our previous study, we found that

the topical application of EGCG could improve AD-like skin lesions of NC/Nga mice by

suppressing the macrophage migration inhibitory factor (MIF) and other T helper (Th) 1-related

cytokines. MIF has been reported to be one of the most crucial immune-regulatory cytokines in

the pathogenesis of AD. Recently, it has been re-evaluated as pro-inflammatory cytokines, and

the over-expression of MIF stimulates Th1, and thereby prolongs an exaggerated inflammatory

response. From these evidences, it is conceivable that MIF contributes to the dysregulation seen

in the inflammatory and the immune responses in AD. However, so far, few experiments have

assessed the effect of EGCG in MIF-induced inflammation and immune deviation in keratinocytes

in vitro. The aim of this study was to assess the anti-inflammatory effect of EGCG and to evaluate

how MIF affects Th-related chemokine and cytokine expression on keratinocytes. First, HaCaT cell

growth induced by various concentrations of EGCG treatment was monitored using the 3-(4,5-

dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide colorimetric assay. Second, to determine

the anti-inflammatory effect of EGCG, HaCaT cells were stimulated with recombinant TNF- withα

or without various concentrations of EGCG. Finally, to determine whether MIF can affect Th-related

chemokines and cytokines, and to determine whether EGCG can regulate the reactions, HaCaT

cells were also stimulated with recombinant MIF with or without various concentrations of EGCG.

RNA and protein levels of MIF, IL-8, and Th-related chemokines and cytokines were measured

by using RT-PCR, Western blot, ELISA and immunofluorescence staining. EGCG treatment did

not significantly affect cell viability, and it was not cytotoxic to the HaCaT cells. EGCG suppressed

recombinant TNF- -induced MIF and IL-8 expression on HaCaT cells in a dose- dependent fashionα

(p < 0.05). Interestingly, Th1-related chemokines (CXCL9, CXCL10, CXCL11) were significantly

up-regulated when treated with recombinant MIF, compared to no treatment (p < 0.05). These results

demonstrate that EGCG has an anti-inflammatory effect by regulating MIF-induced Th-related

chemokines and cytokines in human HaCaT cells.

- 112 -

P-20

Homoisoflavanone prevents allergic responses by blocking degranulation

mast cells through the inhibition of FceRI signaling pathways

Yunsang Lee, Seulgi Hur and Tae-Yoon Kim



Homoisoflavanone isolated from Cremastra appendiculata Makino is known to be involved in

anti-angiogenesis and cell cycle arrest. However, other functions of the homoisoflavanone have not

been investigated. In this study, we determined the anti-allergic effects of homoisoflavanone. For

in vitro experiments, two mast cell lines were used. Treatment of homoisoflavanone inhibited the

release of histamines and b-hexosaminidase. In addition, the production of leukotriene B4,

prostaglandin D2, interleukin (IL)-8, IL-6 and tumor necrosis factor-alpha (TNF-a) was also

inhibited. To analyze the anti-allergic effects of homoisoflavanone in vivo, we induced ear swelling

by compound 48/80 and anti-IgE antibody in mice and attempted to demonstrate whether

homoisoflavanone suppressed ear swelling. Homoisoflavanone inhibited ear swelling up to 53%.

Furthermore, an IgE-mediated passive cutaneous anaphylaxis reaction was also prevented. Finally,

we showed that the anti-allergic effects occurred through the inhibition of FceRI signaling pathways.

In vitro and in vivo anti-allergic effects of homoisoflavanone imply the possible therapeutic

application of homoisoflavanone in allergic diseases

- 113 -

P-21

Effects of corticotropin-releasing hormone on cytokine expression in T cells

Sang Ho Oh, M.D.1,3, Chang Ook Park, M.D.2,3, Ji Young Kim, MS1, Wen Hao Wu, Ph.D.1,

Kwang Hoon Lee, M.D., Ph.D.1

1Department of Dermatology & Cutaneous Biology Institute, Yonsei University College of Medicine, Seoul;2Department of Dermatology, The Armed Forces Byukjae Hospital; 3Both Authors Contributed Equally to

the Study

Corticotropin releasing hormone (CRH) is the central regulating hormone of the HPA axis, which

eventually synthesizes glucocorticoid as a reaction to stress. CRH is not only released from the

central nervous system, but also from various cells of the local tissues, and its receptors also are

distributed in peripheral tissues. Furthermore, CRH is related to the development and aggravation

of several cutaneous diseases including urticaria and atopic dermatitis (AD). We postulated that

CRH might directly affect immune cells, such as T cells, which is of key effector cells to the

immune system. The purpose of this study was to identify the isoforms of CRH receptor (CRH-R)

on T cells, compare the difference in expression of CRH-R on T cells between AD patients and

healthy controls (HCs), and evaluate the direct effect of CRH on Th1, Th2, and regulatory T (Treg)

cells. CRH-R1/R2 proteins and mRNAs for CRH-R1 , 1 , and CRH-R2 were expressed on T cells.α β α

T cells from patients with AD expressed significantly lower levels of CRH-R1/R2 than HCs. CRH

upregulated IL-4 production by Th2 cells in HCs, but not AD patients. However, CRH downregulated

IFN- production by Th1 cells in HCs, but not AD patients. CRH also affected FoxP3-negativeγ

inducible Treg cells producing IL-10 negatively in both HCs and AD patients, and IL-10 production

significantly decreased after CRH treatment especially in patients with AD. Our results suggest

that CRH-mediated immunoregulatory mechanism between normal state and stress-aggravated

disease state may be different and these diverse responses against stress could explain partly

stress-related exacerbation mechanism in AD.

Key Words: Corticotropin-releasing hormone, Th2 cell, regulatory T cell, atopic dermatitis

- 114 -

P-22

The role of ROS produced in XS106 dendritic cells treated by benzalkonium

chloride

Jeong Hwan Je, Dong Hyun Kim, Dashlkhumbe Bayamba, Tae Kyun Kim, Jin Mo Park,

Hyo Jin Noh, Min-Geol Lee


Medicine

Reactive oxygen species (ROS) are considered to be secondary messengers that activate the cell

signaling pathway in inflammatory cells. ROS play important roles in a number of stages during

immunologic responses, including the maturation of dendritic cells (DCs), the interaction of DCs

with T cells, and the activation of T cells. Like such, ROS produced by DCs act as vital ingredients

in the pathogenesis of contact hypersensitivity.

Our previous study showed that allergens and irritants lead to the production of ROS by XS106

DCs. ROS from 2,4,6-trinitrobenzene sulfonic acid (TNBS)-treated XS106 DCs led to an increase

in IL-12 secretion, strongly supporting the role of ROS in contact hypersensitivity. Various

antioxidants were capable of inhibiting the production of ROS in TNBS-treated XS106 DCs.

However, ROS produced by the irritant benzalkonium chloride (BKC)-treated XS106 were different

from those of the TNBS-treated XS106 cell. In light of this finding, we investigated the role of

ROS produced by XS106 DCs in the presence BKC and the results are as follows;

1. ROS were produced from the BKC-stimulated XS106 DCs in a time-dependent manner (1, 2,

6, 12, 24 hr) and in a concentration-dependent manner (2.5, 5, 10, 20, 30 M).μ

2. When exposed to the antioxidants glutathione, catalase, and vitamin E, the production of ROS

was inhibited in the XS106 DCs treated with 30 M BKC for an hour.μ

3. ROS produced in BKC-treated XS106 DCs did not take part in the initiation of apoptosis,

in the change of surface molecules, nor in the expression of p38. They did influence, however,

the increase in the secretion of TNF- by XS106 DCs.α

- 115 -

P-23

Cigarette Smoke-induced Egr-1 regulates the expression of the Cyr61 in

Human Skin Dermal Fibroblasts

Ji Na Kim1, Sang Hoon Jeong

1, Yoon-Hee Park

1, Sang Min Yi

2, Jae Hwan Kim

2, Jae Eun Choi

2,

Il-Hwan Kim2, Young Chul Kye

2, Sang Wook Son

2

1Laboratory of Cell Signaling and Nanomedicine, Korea University College of Medicine, Seoul;2Department of Dermatology and Division of Brain Korea 21 Project for Biomedical Science, Korea


Tobacco smoke is known to be an element contributing to accelerated premature skin aging.

Cysteine-rich 61 (Cyr61) is a member of the connective tissue factor CCN (Cyr61, CTGF, Nov)

family and early growth response-1 (Egr-1) is a generally expressed member of the zing-finger

family of transcription factors. To investigate the regulatory potential of Egr-1 on the expression

of Cyr61 by smoking, this study examined the hypothesis that cigarette smoke-induced Egr-1

induces the expression of Cyr61 in human skin dermal fibroblasts (HSDF).

HSDF was exposed to different concentrations of CSE for 24 hours, and then MTT assay was

used for detection of cell proliferation. By Western blot and RT-PCR experiments, our results showed

that CSE induces a transient synthesis of Egr-1 in HSDF. We also observed the immunostained

Egr-1 proteins were mainly localized from the cytoplasm to the nucleus after CSE treatment by

immunocytochemical analyzes. Cyr61 mRNA and protein levels were markedly increased in a

time-dependent manner after CSE exposure. After being transfected with Egr-1 overexpression

vector, HSDF showed an increased activity of Cyr61 promoter in a dose-dependent manner. Using

Egr-1 interfering RNA, we confirmed that CSE induced Cyr61 expression was dependent on Egr-1

expression. Our data demonstrated that Egr-1 was activated through the mitogen-activated protein

(MAP) kinase pathways after CSE exposure in HSDF.

This study indicates that the MAPK-Egr-1-Cyr61 pathway may contribute to the premature skin

aging by smoking.

- 116 -

P-24

Expression of Wnt5a, CYR61 and HSP90 in the human skin treated with

ablative fractional resurfacing CO2 laser treatment validated by gene

expression profiling

Oun Jae Park, Hana Bak, Chong Hyun Won, Sung Eun Chang, Mi Woo Lee, Jee Ho Choi,

Kee Chan Moon

Asan Medical Center, Korea

To produce the potential benefit of ablative skin resurfacing, ablative fractional photothermolysis

(AFR) CO2 laser is under much clinical investigations but without knowledge of molecular

mechanism. For elucidating the mechanism of AFR laser, we assayed for changes in gene expres-

sions by microarray analyses for investigation of the changes of the gene expressions after AFR

CO2 laser treatment on the human skin. We used RT-PCR to validate modulation of candidate

genes. In vitro, fibroblasts exposed for 2 hours to a temperature range of 44-50C was assayed as

the same methods. The majority of significantly changed genes were Wnt5a, cysteine-rich

angiogenic inducer 61 (Cyr61), heat shock protein (HSP) 90 and aquaporin 3. Confocal laser

scanning microscopy was used for investigation of expression of these proteins in the skin after

the laser treatment. We found the same manner in the expression of Wnt5a, Cyr61 and HSP90

in the skin. These data suggest that AFR laser treatment might induce Wnt5a, Cyr61 and HSP90

in the skin and those proteins might deeply associated with beneficial effects of the laser treatment.

- 117 -

P-25

Horse oil induces the increased expression of IL-10 in HaCaT cells

Sung-Ae Kim, Min-Chul Kang, Jun-Il Kwon, Jae-We Cho, Kyu-Suk Lee


Horse oil has been used long time as the folk medicine of many Asian countries such as Korea,

Mongol, China, India and Japan. Horse oil has been used for anti-bacterial, anti-inflammatory, and

anti-pruritic purposes in skin. However, it is still largely unknown whether horse oil modulates

the expressions of inflammatory cytokines in HaCaT cells, and bactericidal or bacteriostatic effect

on P. acnes. Horse oil was purchased from Sansae-mi Company, Jeju Island, and Republic of Korea.

In this study, we studied bactericidal effect of horse oil on P. acnes and immunomodulatory effect

on expressions of IL-1, IL-6, IL-8, IL-10, TNF- , and COX-2 in HaCaT cells. Our data showed theα

horse oil exerted bacteriostatic effect on P. ances, evidenced by clear zone around horse oil disc

in P. acnes-cultured plate. In addition HaCaT cells were treated by horse oil, and then expression

levels of inflammatory cytokines were analyzed by RT-PCR or real time PCR. Our data showed

the horse oil induced the increased expression of IL-10 in HaCaT cells, but not markedly

modulated expressions of IL-1, IL-6, IL-8, TNF- , and COX-2. Taken together, horse oil exertedα

the bacteriostatic effect on P. acnes and up-regulation of IL-10 in HaCaT cells, thereby this agent

may play roles for improving acne in skin.

- 118 -

P-26

Simvastatin Inhibits Transforming Growth Factor-β1 Induced Collagen Type

I and CTGF Expression in Keloid Fibroblasts

Je-Ho Mun, M.D.1, Young-Mi Kim

2, Hyun-Chang Ko, M.D.

1, Byung-Soo Kim, M.D.

1,

Jae-Ho Kim2, Moon-Bum Kim, M.D.

1

Department of 1Dermatology, 2Physiology, School of Medicine, Pusan National University, Busan, Korea

Simvastatin, which inhibit 3-hydroxy-3-methylglutaryl coenzyme-A (HMG CoA) reductase, is

used to lower cholesterol levels. Accumulating evidence reveals its immunomodulating and

anti-inflammatory effects to prevent cardiovascular disease. In addition, the beneficial effect of

statins on organ fibrosis has been reported. However, functional effect of statins on dermal fibrosis

in keloids has not been explored.

To investigate the effect of simvastatin on transforming growth factor (TGF)- 1-inducedβ collagen

type I and connective tissue growth factor (CTGF) expression in human keloid fibroblasts.

Keloid fibroblasts were cultured and exposed to different concentration of simvastatin in the

presence of TGF- 1. We evaluate the effect of simvastatin on TGF- 1-induced collagen and CTGFβ β

expression in keloid fibroblasts. The proteins of collagen type I, CTGF, -smooth muscle actinα

(SMA) and phosphorylation of smad-2 and smad-3 were assessed by Western blotting. The effects

of geranylgeranyl pyrophosphate (GGPP) and farnesyl pyrophosphate (FPP), which are the

cholesterol pathway intermediates of lipids down-stream from the HMG CoA reductase, were also

examined. The effect of simvastatin on cell viability was evaluated by the colorimetric conversion

of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide.

Simvastatin suppressed TGF- 1-induced collagen type I expression in keloid fibroblasts in aβ

concentration-dependent manner. Furthermore, simvastation pretreatment inhibited expression of

CTGF and the myofibroblast specific marker, -SMA. The phosphorylation levels ofα TGF-β

1-induced smad-2 and smad-3 were abrogated by pretreating of the cells with simvastatin. The

inhibition of collagen type I and CTGF expression by simvastatin was reversed by GGPP, not by

FPP. However, cell viability was not affected by simvastatin treatment.

Our data suggest that simvastatin is an effective inhibitor of TGF- 1-induced collagen type Iβ

and CTGF expression in Keloid fibroblasts. Simvastatin may be a promising therapeutic agent for

keloids.

- 119 -

P-27

SOD3 expression up-regulated by PKC-delta inhibits cell proliferation in

melanoma via the Stat1-p21 pathways

Hyun Yoo, Yunsang Lee, Byeongwook Jeon and Tae-Yoon Kim

Laboratory of Dermato-Immunology, Catholic Research Institute of Medical Science, College of Medicine, The

Catholic University of Korea, Seoul Korea

The physiological role of IFNr has been implicated in the modulation of tumor cell proliferation

and apoptosis. It has been shown that IFNr induces PKC-delta (PKCd) induced inhibition of tumor

cell proliferation and up-regulates SOD3 expression. However, the details of the mechanism have

not been well elucidated. In this study we investigated how PKCd and SOD3 interact with each

other to inhibit tumor cell proliferation. To determine the relationship between PKCd and SOD3,

we monitored SOD3 expression in the PKCd over-expressed human melanoma and explored the

signaling pathways of SOD3. We observed a rapid increase in SOD3 expression in PKCd

transfected cells while the PKCd-induced up-regulation of SOD3 was attenuated by pretreatment

with PKC specific inhibitors. Additionally, we demonstrated that SOD3 drastically suppressed lung

metastasis in an SOD3 transgenic mouse via the Stat1-p21 expression. Finally, we confirmed that

the transfection of SOD3 expression vector enhanced IFNr-induced apoptosis. These results indicate

that IFNr directly induced SOD3 expression via activation of PKCd pathways in human melanoma.

Taken together, our findings suggest that PKCd-induced over-expression of SOD3 inhibits

melanoma cell growth via activation of the Stat1-p21 pathway.

- 120 -

P-28

Differential expression of ABO antigens in normal and altered skin conditions

Dong-Hun Lee, Jang Hee Oh, Ji Yong Jung, In Ho Kwon, Se Rah Lee, Yeon Kyung Kim,

Hyun Sun Yoon, Eun Young Seo, and Jin Ho Chung


Aging Research, Clinical Research Institute, Seoul National University Hospital; Institute of

Dermatological Science, Medical Research Center, Seoul National University, Seoul, Korea.

Since its discovery by Karl Landsteiner in 1900, ABO blood group antigens have played a pivotal

role in transfusion medicine. Recently, their possible roles in infection and cancer have been

proposed; however, their role in skin remains elusive. To elucidate their expression and function

in skin, immunohistochemical analyses using monoclonal anti-A, B, or, H antibody were performed

for the specimens diagnosed as psoriasis, atopic dermatitis, and those irradiated with 2-MED

ultraviolet (UV), in addition to normal control. In normal skin, A/B antigen was mainly expressed

in stratum granulosum, while H antigen was in stratum spinosum. In psoriasis and atopic

dermatitis, A or B antigen expression showed an appreciable decrease in stratum granulosum with

a slight increase in stratum spinosum, and H antigen was extensively stained in stratum spinosum.

In acute UV-irradiated skin, A/B antigen expression in stratum granulosum were decreased, but

H antigen expression showed marked increase in stratum spinosum and stratum basale. Real-time

RT-PCR revealed that transferase A and B decreased after the UV irradiation, whereas related

glycosyltransferase including FUT1, B4GALT1,2,3,4, B3GNT5, B4GALT6 increased at 24h after the

irradiation. In conclusion, the expression of ABO blood group antigen showed a differential

distribution and intensity according to skin disorders, suggesting that ABO blood groups might

be implicated in the pathogenesis of various skin diseases in the aspect of differentiation and

inflammation.

Key Words: blood group, immunohistochemistry, ultraviolet

- 121 -

P-29

The role of aryl hydrocarbon receptor on UVB-induced MMP-1 expression

in human skin cells

Jeong Yoon Lee, Chi-Hyun Park, Jang-Hee Oh, Jin Ho Chung


Aging Research, Clinical Research Institute, Seoul National University Hospital;

Institute of Dermatological Science, Medical Research Center, Seoul National University, Seoul, Korea.

The aryl hydrocarbon receptor (AhR) is known to be activated by environmental xenobiotics and

ultraviolet (UV), and plays important roles in inflammation and skin diseases. However, the role

of AhR on UV-induced MMP-1 expression has not been elucidated. In this study, we found that

expression of AhR mRNA levels were increased in forearm skin compared to those in buttock

skin of the same individual and that AhR mRNA expression was increased in UV-irradiated mouse

skin. Furthermore we found that AhR expression was also induced by UV in human skin

fibroblasts and HaCaT cells. Then, we investigated the role of AhR MMP-1 expression induced

by UV in HaCaT cells. The UV-induced MMP-1 expression was significantly decreased by pretreat-

ment with -Naphthoflavone, an AhR inhibitor and by transfection of specific AhR siRNA. Takenα

together our results indicate that AhR play an important role on UV-induced MMP-1 expression

in human skin fibroblasts and keratinocytes. Further analysis of these features will be essential

in understanding signaling pathway of UV-induced MMP-1 expression.

- 122 -

P-30

Investigation of papulopustular eruptions caused by cetuximab treatment

shows altered differentiation markers and increases in inflammatory

cytokines

Gyeong-Hun Park1, Seung-Seog Han

2, Mi-Woo Lee

1, Jee-Ho Choi

1, Kee-Chan Moon

1

1Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul;2Dermatology Clinic, Seoul, Korea

Epidermal growth factor receptor (EGFR) critically regulates tumour cell division, survival and

metastasis. Agents that inhibit EGFR have been used in the treatment of advanced- stage

malignancies, but cause variable cutaneous side-effects, most often papulopustular eruptions and

xerosis.

We assayed expression of inflammatory cytokines [interleukin (IL)-1 , tumour necrosis factorα

(TNF)- , interferonα (IFN)- , human leucocyte antigenγ (HLA)-DR and intercellular adhesion

molecule (ICAM)-1], differentiation markers (filaggrin, involucrin and loricrin) and phosphorylated

EGFRs (pEGFRs) in papulopustular eruptions to determine the association between these markers

and the eruptions caused by cetuximab.

We performed biopsies and immunohistochemical studies from the papulopustular lesions of

twelve patients with colon cancer who had received cetuximab treatment.

Filaggrin expression decreased and expression of involucrin, various inflammatory markers (IL-1

, TNF- , ICAM-1 and HLA-DR) increased and the expression of pEGFR was markedlyα α

downregulated in papulopustular eruptions. In perilesions, decreased pEGFR expression was noted

in hair follicles compared with interfollicular epidermis. The expressions of both IL-1 and TNF-α α

were slightly increased in perilesions as in the lesions.

The early inflammatory events (IL-1 and TNF- expression) seen, and the lack of pEGFR inα α

perilesional follicles, indicate that inflammatory events induced by EGFR inhibition may initiate

papulopustular eruptions along with the altered differentiations. The decrease of filaggrin may

contribute to the pathogenesis of the xerosis caused by cetuximab.

- 123 -

P-31

Identification of the filaggrin gene polymorphisms with ichthyosis vulgaris in

Korean patients

Dong Ha Kim1, In Su Kim

1, Jin Woong Lee

1, Kwang Ho Yoo

1, Mi Sook Jeong

2, Kim Eun Joo

2,

Beom Joon Kim1, Myeung Nam Kim

1, Kui Young Park

1, Kapsok Li

1, Seong Jun Seo

1,

Chang Kwun Hong1

Department of Dermatology, Chung-Ang University College of Medicine1, Chung-Ang Medical Research

Center2

Filaggrin (FLG) is a key protein that facilitates the formation of a skin barrier by forming a

stratum corneum. Mutations in FLG in ichthyosis vulgaris (IV) patients have recently been reported

in many studies, and it is known that FLG and atopic dermatitis (AD) are significantly correlated.

There are some differences between FLG mutations identified in Asians and Europeans, and few

FLG mutations in Asians are overlapping with each other. Furthermore, new types of mutations

have recently been reported in Japan. In this study, FLG mutations in South Korean IV patients

are examined. DNAs were harvested from blood samples of three IV patients. After each exon

region was distinguished by subregion, FLG mutations that were unique to Koreans were

examined using PCR and the sequencing method. Two new SNPs (p.G2454R and p.R2787H) were

found in the repeat 7 - 8 regions, which were analyzed completely. In all three specimens, repeat

10 of exon 3 was found to have consisted of repeats 10.1 and 10.2, the patterns of which were

similar to those of the Japanese. Though no new mutations or meaningful nonsense mutations

were identified, new SNPs that are unique to Koreans were found. Studies on FLG mutations that

are unique to Koreans could provide a treatment method for IV patients or patients with AD.

In this light, more studies are required.

- 124 -

P-32

The Effect of Calcipotriol on the Expression of Human βDefensin-2 and

LL-37 In Cultured Human Keratinocytes

Woo Sun Jang1, Hyun Kyu Kim

1, Juhee Park

1, Hye In Lee

1, Mi Sook Jeong

2, Eun Joo Kim

2,


1, Kui Young Park

1, Kapsok Li

1, Seong Jun Seo

1,

Chang Kwun Hong1

1Department of Dermatology, Chung-Ang University College of Medicine, 2Chung-Ang Medical Research

Center

Vitamin D has been reported to regulate innate immunity by controlling the expression of

antimicrobial peptides (AMPs). We investigated the effect of calcipotriol on the expression of AMPs

in human cultured keratinocytes. Keratinocytes were treated with lipopolysaccharide (LPS), TNF- ,α

Calcipotriol and irradiated with UVB, cultured, and harvested. To assess the expression of human

beta defensin-2 and LL-37 in the control group, not exposed to any stimulants, the experimental

group was treated with LPS, TNF- or UVB, and another group was treated again with calcipotriol;α

reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemical

staining were performed. In the experimental group treated with LPS, UVB irradiation, and TNF- ,α

the expression of -defensin and LL-37 was increased more than in the control group, and thenβ

decreased in the experimental group treated with calcipotriol. Calcipotriol suppressed HBD-2 and

LL-37, which were stimulated by UVB, LPS, and TNF- .α

- 125 -

P-33

Effect of Topical Application and Intraperitoneal Injection of Oregonin on

Atopic Dermatitis (AD) in NC/Nga Mice

Woo Sun Jang1, Hyun Kyu Kim

1, Juhee Park

1, Hye In Lee

1, Mi Sook Jeong

2, Eun Joo Kim

2,


1, Kui Young Park

1, Kapsok Li

1, Seong Jun Seo

1,

Chang Kwun Hong1

Department of Dermatology, Chung-Ang University College of Medicine1, Chung-Ang Medical Research

Center2

The diarylheptanoid chemical, Oregonin (ORE), isolated from the bark of the Alnus genus plant

of Alnus japonica Steudel that grows natively in Korea, has been known to exert antioxidative,

anti-inflammatory, anti-cancer, and immune response inhibitory effects. It was thus expected that

ORE would exert a beneficial effect in the treatment of AD. We used an in vivo AD animal model,

namely the NC/Nga mice, and by applying ORE onto the animals through skin application as

well as intraperitoneal injection. The following categories of clinical evaluation, Th2 cytokines IL-4,

5 and 13 values, serum IgE levels, serum eosinophil levels, and mRNA and protein expression

levels of iNOS and COX-2, were evaluated from the ORE application and intraperitoneal injection

groups. The effects of ORE on AD in Nc/Nga mice were confirmed as being similar to the positive

control group, while a significant difference with the negative control group was observed.

The results presented in this report suggest that ORE might be beneficial in the treatment of

AD.

- 126 -

P-34

Differential expression patterns of MMPs and their role in the invasive

properties of epithelial premalignant tumors and invasive squamous cell

carcinoma

Mi Ryung Roh, M.D.1, Hang Ran Chang, Ph.D.

2, Ji Eun Kwon, M.D.

1, Sun-Young Rha, M.D., Ph.D.

2,

Kee Yang Chung, M.D., Ph.D.1

1Department of Dermatology and Cutaneous Biology Research Institute, Department of Pathology and2Department of Medical Oncology, Yonsei University College of Medicine, Seoul, Korea

Co-expression of several members of the matrix metalloproteinase (MMP) family is characteristic

of human malignant tumors. MMPs are thought to be involved in the process of destruction of

basement membranes and stromal invasion by neoplastic epithelial cells.

In order to investigate the role of MMPs in cutaneous oncogenesis, we compared the expression

of MMP-2, MMP-9, MMP-14 and TIMP-2 in epithelial premalignant tumors and invasive squamous

cell carcinomas.

A study of 23 normal skin, 29 Bowen’s disease (BD), 61 squamous cell carcinoma (SCC) samples

for MMP-2, MMP-9, MMP-14 and TIMP-2 expression was carried out using immunohistochemical

staining.

When compared with normal epithelium, SCC and BD showed higher expression of MMP-14

with different expression patterns. SCC showed high expression of MMP-14 in the invasive front

of the tumor, while BD showed higher expression around the tumor cells in the epithelium. SCC

showed higher MMP-2 expression compared to normal epithelium and BD. MMP-9 was not

detected in BD or SCC but detected only in the basal layer of the normal epithelium.

The complex expression of MMPs seems to have an important role in the molecular biology

of cutaneous oncogenesis. Their expression by different tumors may be of clinical interest to be

used as indicators of tumor aggressiveness and invasion.

- 127 -

P-35

Expression of ATF3 on skin cancer

Myoung-Shin Kim1, Seung-Gyun In

2, Hyung-Min Lee

1, Chong-Hyun Won

1, Sung-Eun Chang

1,

Mi-Woo Lee1, Jee-Ho Choi

1, Kee-Chan Moon

1

1Department of Dermatology, Asan Medical Center, University of Ulsan, College of Medicine,2Department of Dermatology, Inha University Hospital

Activating transcription factor 3 (ATF3) is a member of the ATF/cyclic AMP response element-

binding (ATF/CREB) family of transcription factors. It is known as an adaptive-response gene and

has an oncogenic role in various cancer developments. But to our knowledge nothing is known

about the possible role of ATF3 in skin cancer. So we investigated expression of ATF3 in basal

cell carcinoma (BCC), squamous cell carcinoma (SCC) by immunohistochemical method.

In this study, no ATF3 expression was detectable in normal skin and BCC. Immunohisto-

chemistry revealed expression of ATF3 in SCC, suggesting that BCC and SCC might have different

mechanism of cancer development. In addition there is higher expression of ATF3 in metastatic

SCC and SCC in immunocompromised hosts.

These data suggest that ATF3 may play an oncogenic role in skin cancer. ATF3 can be a tumor

marker in SCC.

- 128 -

P-36

Expression of matrix metalloproteinases and their role in the invasive property

of squamous cell carcinoma

Mi Ryung Roh, M.D.1, Jin Young Jung, M.D.

1, Su Hyun Lee, M.D.

1, Keun-Jae Ahn, Ph.D.

1,

Hyun Sook Kim1, Sun-Young Rha, M.D., Ph.D.2, Kee Yang Chung, M.D., Ph.D.1

Department of 1Dermatology and Cutaneous Biology Research Institute, 2Medical Oncology, Yonsei


Metalloproteinases (MMPs) are thought to be involved in the process of the destruction of

basement membranes and stromal invasion by neoplastic epithelial cells. MMP- 14 forms a

trimolecular complex on the cell surface containing tissue inhibitor of metalloproteinases 2

(TIMP-2) and pro MMP-2, resulting in proMMP-2 activation and release.

In order to investigate the role of MMPs in the invasive property of squamous cell carcinoma,

we measured and compared MMP-2, MMP-9, TIMP-2 and MMP-14 mRNA, protein, and activity

by real-time RT-PCR, gelatin zymography and western blotting in 3 human squamous cell

carcinoma cell lines. The invasive property of each squamous cell carcinoma cell lines were

evaluated with invasion assays using transwell filters.

High expression of MMP-14 was detected in SCC-9 cell line. High expression of MMP-2 was

detected in SCC-25 cell line. Low expression of MMP-9 was detected in SCC-9 cell line but there

was no expression of MMP-9 in SCC-15 and 25 cell line. SCC-9 cell line showed the highest TIMP-2

expression. SCC-25 cell line showed the highest invasiveness and SCC-15 cell line showed the

lowest invasiveness.

The high level expression of MMP-14, MMP-2, and low expression of TIMP-2 seem to correlate

with the invasive property of squamous cell carcinoma in vitro.

- 129 -

P-37

Association of thymic stromal lymphopoietin gene -847C>T polymorphism in

generalized vitiligo

Kyung Ah Cheong1, Soo-Cheon Chae

2, Yong-Shin Kim

3, Hyok Bu Kwon

1, Hun-Taeg Chung

3

and Ai-Young Lee1

1Department of Dermatology, Dongguk University Ilsan Hospital, Goyang, Korea2Department of Pathology, School of Medicine, Wonkwang University, Iksan, Chonbuk,Korea;3Genome Research Center for Immune Disorders, School of Medicine, Wonkwang University, Iksan,

Chonbuk, Korea

Thymic stromal lymphopoietin (TSLP) induces naïve CD4+ T cells to produce Th2 cytokines,

however, TSLP receptor knockout could induce strong Th1 responses with low production of Th2

cytokines. This study examined whether a functional TSLP polymorphism associated with vitiligo.

One hundred sixty Korean patients with vitiligo and 568 healthy Korean individuals were

examined for the four SNPs of TSLP gene. Luciferase activity was measured for promoter assay.

The genotype and allele frequencies of -847C > T polymorphism were lower in vitiligo patients

compared with controls, whereas those of wild type were higher (p=0.004, p = 0.017, respectively).

None the less, the promoter activity of -847C decreased significantly (p = 0.013) compared with

-847T, expecting lower TSLP mRNA levels in the polymorphism. Overall, C allele at the TSLP

-847C > T polymorphism may increase susceptibility to generalized vitiligo through decreasing

TSLP mRNA expression levels, in turn, inducing immune responses of Th2-suppression.

Key words: TSLP -847C>T polymorphism; promoter activity, lower TSLP mRNA levels, C allele,

susceptibility to generalized vitiligo

- 130 -

P-38

Expressions of NOTCH signaling pathway in psoriasis

Chang Sung Eun1, Moon Kee Chan1, Choi Jee Ho1, Lee Mi Woo1, Won Chong Hyun1,

Chang Deok Kim2, Seung Hyun Bang

1

1Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine,2Department of Dermatology, School of Medicine, Chungnam National University

Psoriasis is a chronic inflammatory skin disease characterized by complex alteration in epidermal

growth and differentiation. NOTCH signaling, ATF1, ATF3, Wnt5a and Hes1 control a number

of cellular processes including cell proliferation, differentiation and cell fate decision. These signals

are direct or indirect regulator of keratinocyte growth, differentiation and considered to be associated

with psoriasis pathogenesis. To investigate the expression NOTCH signaling, ATF1, ATF3 and

Wnt5a, psoriatic lesions are obtained and the expressions of these signals were evaluated.

Immunohistochemistry showed that the expression of Notch1, Notch2, Delta-like1, ATF3 and

HES1 were significantly decreased in psoriatic lesions as compared with normal skin. Consistent

with, RT-PCR showed that mRNA levels for Notch2, Delta-like1, ATF3 and HES1 were markedly

reduced in posriatic lesions. However RT-PCR of ATF1 and Notch1 showed no significant

difference between normal skin and psoriatic lesions. Wnt5a was upregulated in psoriatic lesions.

NOTCH-associated pathway is significantly decreased in psoriatic lesions except Wnt5a signal

which is a possible non-canonical pathway of NOTCH.

Our data strengthens the notion that these signals are functionally involved in psoriasis suggesting

these systems may be a therapeutic target for treatment of psoriasis

- 131 -

P-39

Sphingosylphosphorylcholine-induced interleukin-6 production is mediated by

protein kinase C and p42/44 extracellular signal-regulated kinase in human

dermal fibroblasts

Dae-Kyoung Choi1, Kyung-Cheol Sohn

1, Yoo Bin Kwon

1, Nari Kim

1, Ah Young Cho

1,

Young Ho Lee2, Tae-Jin Yoon

3, Young Lee

1, Chang Deok Kim

1, Jeung-Hoon Lee

1

1Department of Dermatology, School of Medicine, Chungnam National University, Daejeon;2Department of Anatomy, School of Medicine, Chungnam National University, Daejeon;3Department of Dermatology, School of Medicine, Gyeongsang National University, Jinju, Korea

Sphingosylphosphorylcholine (SPC) has been reported as a novel lipid mediator that exerts

various actions on wound healing process. The aim of this study is to evaluate the involvement

of interleukin-6 (IL-6) in SPC-induced wound healing acceleration. We performed immuno-

histochemisty analysis to demonstrate the IL-6 induction by SPC. To analyze the signaling events,

skin fibroblasts were treated with SPC, and then RT-PCR, ELISA, and Western blot analyses were

carried out. SPC markedly induced interleukin-6 (IL-6) expression in rabbit ear wound. SPC also

induced IL-6 expression at both the transcriptional and translational levels in human dermal

fibroblasts cultured in vitro. SPC rapidly phosphorylated p42/44 extracellular signal-regulated

kinase (ERK). Pretreatment with PD 98059, a specific MAPK kinase 1/2 inhibitor, markedly

suppressed SPC-induced IL-6 expression in a dose-dependent manner. Protein kinase C (PKC)

activation by phorbol myristate acetate (PMA) potentiated IL-6 mRNA expression, whereas PKC

inhibition by bisindolylmaleimide blocked SPC-induced p42/44 ERK phosphorylation and IL-6

expression. These results suggest that SPC-induced IL-6 production is mediated by PKC-dependent

p42/44 ERK activation in human dermal fibroblasts cultured in vitro.

- 132 -

P-40

Alteration of extracellular matrix modulators in photoaged skin after

combined laser, light and radiofrequency treatment

Chae Hwa Kim, Jeong Eun Kim, Gyeong Hun Park, Chong Hyun Won, Sung Eun Chang,

Mi Woo Lee, Jee Ho Choi, Kee Chan Moon

Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine

As the demand for non-invasive procedures in the treatment of photoaged skin, radiofrequency

(RF) combined devices have recently emerged. The purpose of this study is to evaluate the safety

and efficacy of triple combination treatment and alteration of extracellular matrix modulators.

Ten women received four treatment at 3-week interval with triple tips of RF-based device. IPL

combined RF, infrared combined RF and diode laser combined RF tips were sequentially

applicated to the treated side. All subjects were taken clinical photographs every visit and the

changes were evaluated. Two-millimeter skin punch biopsies were obtained from both side of

treated and untreated face at 1 month after the last treatment.

In terms of clinical assessment, 80% of patients were identified to have some degree of improve-

ment of the treated side 1 month after their last treatment. RF-combined triple combination

treatment led to increase the level of type collagen and elastin and decrease the level of

cystein-rich 61(CYR61/CCN1).

RF-based triple combination treatment can be used effectively and safely for the treatment of

photoaged skin. This method may effectively combine three different energy source and may

induce active dermal remodelling process.

- 133 -

대한피부연구학회 회칙

제 1장 총 칙

제 조 명칭 본 학회는 대한피부연구학회 라1 ( ) (The Korean Society of Investigative Dermatology)

칭한다.

제 조 목적 본 학회는 피부과학의 기초 및 임상 연구를 촉진하여 피부과학 발전에 기여함을2 ( )

목적으로 한다.

제 조 사업 본 학회는 제 조의 목적 달성을 위하여 다음과 같은 사업을 수행한다3 ( ) 2 .

학술대회 및 강연회 개최

학회보 및 학회지의 발행

국내 국외의 관계 학술 단체와의 교류 및 제휴,

기타 본 학회 목적 달성에 필요한 사업

제2장 회 원

제 조 자격 본 학회의 회원은 피부과학의 연구에 종사하거나 피부과학 연구에 관심을 가지고4 ( )

본 학회의 취지에 찬동하는 자로서 소정의 입회 수속을 밟고 상임이사회의 심의

및 추천을 받은 후 이사회의 의결을 거친 자로 한다.

제 조 구분 본 학회의 회원은 다음과 같이 구분한다5 ( ) .

정 회 원 피부과학 또는 관련분야의 연구자로서 본 학회 목적에 찬동하는 자로 한다: .

국외회원 외국에서 피부과학 또는 관련분야에 종사하는 자로서 본 학회 목적에 찬동하는:

자는 국외회원이 될 수 있다.

명예회원 피부과학 연구 업적이 탁월하고 본 학회 발전에 공헌이 지대한 자는 명예회원이:

될 수 있다.

단체회원 본 학회의 목적에 찬동하는 연구소는 단체회원이 될 수 있다: .

제 조 의무 회원은 본 학회의 회칙 제규정 및 결의사항을 준수하여야 하고 정회원 국외회원6 ( ) , , ,

및 단체회원은 회비 및 기타의 부담금을 납부할 의무가 있다.

제 조 권리 모든 회원은 본 학회에서 발간하는 학회지를 배부 받을 권리가 있으며 정회원은7 ( )

선거권 피선거권 및 기타 소정의 의결권을 가진다, .

제 조 제명 본 학회의 의무를 준수하지 않거나 본 학회의 명예를 훼손하거나 정당한 이유없이8 ( ) , ,

년 이상 회비를 납부하지 않은 회원은 이사회의 의결을 거쳐 총회의 인준을 받아3

제명할 수 있다.

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제3장 임 원

제 조 구성 본 학회는 회장 명 차기회장 명 이사장9 ( ) (President) 1 , (President-elect) 1 , (Chairman)

명 이사 명 내외 감사 명의 임원을 둔다1 , (Board of Directors) 20 , (Auditors) 2 .

제 조 선임10 ( )

회장 차기회장 감사는 총회에서 선출한다, , .

이사장은 회장의 추천에 의해 총회의 인준을 받는다.

이사 및 상임이사는 이사장이 회장단과 협의하여 선임하고 총회의 인준을 받는다.

제 조 임기 임원의 임기는 년으로 하며 연임할 수 있다 단 회장 및 이사장은 연임할 수11 ( ) 2 . ,

없다 이사의 임기는 년으로 하고 매년 분의 씩 보선 교체한다 전임자의 유고로. 3 3 1 .

인해 보선된 임원의 임기는 전임자의 잔여 임기간으로 한다.

제 조 직무12 ( )

회장은 본 학회를 대표하여 업무를 총괄하고 총회의 의장이 된다.

차기회장은 회장 유고 시 그 직무를 대행하여 현 회장의 임기 후 회장작을 맡는다.

이사장은 이사회의 업무를 총괄하고 이사회 및 상임이사회의 의장이 된다.

이사는 이사회의 구성원이 되며 본 학회 운 의 주요한 사항을 심의한다.

상임이사는 이사회 및 상임이사회의 구성원이 되며 본 학회의 제반 업무를 집행한다.

상임이사의 제반 업무를 보좌하기 위하여 간사를 둘 수 있다 간사는 이사회 및 상임이사회.

에 참석할 수 있다.

감사는 본 학회의 재산 상황과 사업과 관련된 사항을 감사하고 이를 총회에 보고한다.

제4장 회 의

제 조 구분 본 학회에는 총회 이사회 상임이사회를 둔다13 ( ) , , .

제 조 총회14 ( )

정기총회는 년 회 회장이 소집한다 단 정회원 분의 이상의 요구나 이사회의 요청이1 . , 5 1

있으면 임시총회를 소집하여야 한다.

총회는 정회원의 분의 출석으로 성립하고 재적인원 과반수로 의결한다 단 총회가 성립3 1 . ,

되지 않을 때는 총회에 참가 등록한 정회원의 분의 출석으로 성립하고 재적인원 과반3 1

수로 의결한다.

총회는 다음과 같은 사항을 의결한다.

회장 차기회장 감사 선출, ,

이사장 이사 상임이사 인준, ,

예산과 결산

회칙 개정의 인준

기타 이사회에서 제출한 사항

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제 조 이사회15 ( )

이사회는 이사장 이사와 상임이사로 구성하고 회장단 감사 및 간사가 참석할 수 있다, .

이사회는 이사 과반수 출석으로 성립하고 재적인원 과반수로 의결한다.

정기이사회는 년 회 이사장이 소집한다 단 임시 이사회는 이사장이 수시로 소집할 수 있으2 . ,

며 이사 분의 이상의 요구가 있을 때 소집하여야 한다, 3 1 .

이사회는 본 학회의 운 에 필요한 제반 사항을 심의 의결 또는 인준한다, .

제 조 상임이사회16 ( )

상임이사회는 이사장 총무이사 학술이사 간행이사 및 재무이사로 구성하며 본 학회의 운, , ,

에 필요한 제반 사항을 심의하고 업무를 집행한다.

각 상임이사는 다음과 같이 회무를 분담한다.

총무이사 본 회의 관리 회무 및 회원 상호간의 친목 등에 관한 업무 총괄: ,

학술이사 학술대회 및 학술 등에 관한 업무:

간행이사 학회보 학회지 및 기타 간행 등에 관한 업무: ,

재무이사 재정 및 회계 등에 관한 업무:

정보이사 정보 통신 및 홈페이지 관리와 운 에 관한 업무: ,

각 상임이사는 정회원 약간명씩으로 구성된 운 위원회 학술위원회 간행위원회 재무위원, , ,

회 정보위원회를 구성할 수 있다, .

제5장 재 정

제 조 재원 본 학회의 재원은 회비 입회비 찬조금 및 기타 수익금으로 한다17 ( ) , , .

제 조 회계 연도 본 학회의 회계 연도는 매년 정기총회에서 다음 정기총회일까지로 한다18 ( ) .

제 조 감사 본 학회의 수지결산은 감사의 감사를 거쳐 차기 정기총회에 보고한다19 ( ) .

제6장 부 칙

제 조 본 회칙의 개정은 이사회의 심의를 거쳐 총회의 인준을 받아야 한다20 .

제 조 본 회칙에 규정되지 않은 세칙은 일반 관례에 준한다21 .

제 조22

본 회칙은 공포일 년 월 일부터 시행한다(1991 3 23 ) .

본 회칙은 년 월 일부터 개정 시행한다1992 3 21 .





- 136 -

대한피부연구학회 연혁

1991. 2. 2 발기인대회

강남성모병원에서 발기인 인이 참석50

1991. 3. 23 창립총회 및 제 차 학술대회1 르네상스호텔( )

특강연자 : Sadao Imamura (Kyoto Univ.)

박상대 서울대 자연과학대( )

일반연제 편10

제 대 회장단 취임1

회장 김 표 이사장 이정복: , :

1991. 11. 23 제 차 심포지엄1

주제 발표 연제: Interleukin, : 6

강남성모병원

1992. 3. 21 제 차 학술대회2 르네상스호텔( )

특강연자: Jouni Uitto (Thomas Jefferson Univ.)

교육강연 연제 심포지엄 광피부과학 연제 심포지엄 연제2 , 6 , PCR 6 ,

포스터 연제19

제 차 총회에서 회칙개정2

평의원제를 폐지하고 이사장 상임이사제도를 신설,

1992. 11. 7 제 차 심포지엄2 가톨릭의대 대학원 강의실( )

주제 피부세포배양 발표 연제: , : 6

가톨릭의대 대학원 강의실 여명 참석130

대한피부연구학회보 창간

1993. 3. 20 제 차 학술대회3 르네상스호텔( )

특강연자 : Irvin H. Epstein (USCF)

교육강연 연제 구연 연제 포스터 연제6 , 13 , 14

제 대 회장단 취임2

회장 이유신 이사장 윤재일: , :

1993. 11. 6 제 차 심포지엄3 가톨릭의대 대학원 강의실( )

주제 분자생물학 발표 연제: , : 9

국외 초청연자 : Peter Steinert (NIH)

정수일 (NIH)

1994. 3. 19 제 차 학술대회4 소피텔 앰버서더호텔( )

특강연자 : K. Nishioka (Tokyo Medical and Dental Univ.)


- 137 -

1994. 11. 5 제 차 심포지엄4 가톨릭의대 마리아홀( )

주제 광의학 발표 연제: , : 8

대한피부연구학회지 창간호 발간

1995. 3. 18 제 차 학술대회5 쉐라톤 워커힐호텔( )

특강연자 : Roger Allen (University Hospital Nottingham)


제 대 회장단취임3

회장 허원 이사장 노병인: , :

1995. 11. 25 제 차 심포지엄5 가톨릭의대 마리아홀( )

주제 발표 연제: Apoptosis, : 5

국외 초청연자 대학: Kouichi Ikai (Kyoto )

1996. 3. 16 제 차 학술대회6 서울중앙병원( )

특강연자 : Motomu Manabe (Juntendo Univ.)

교육강연 연제 구연 연제 심포지엄 유전질환 연제 포스터 연제4 , 14 , ( ) 6 , 8

1996. 11. 23 제 차 심포지엄 호텔롯데6 ( )

주제 노화와 광노화 발표 연제: , : 13

국외 초청연자 : John J. Voorhees (Univ. of Michigan)

Masamitsu Ichihash (Kobe Univ.)

1997. 3. 4 대한피부연구학회가 대한의학회 준회원으로 인준받음

1997. 3. 15 제 차 학술대회7 서울중앙병원( )

특강연자 : C. E. Orfanos (Free Univ.)

심포지엄 모발 특강연자 : S. Arase (Tokushima Univ.) /

R. Tsuboi (Juntendo Univ.) / A. G. Messenger (Royal Hallamshire Hospital)

김정철 경북대/ ( )

구연 연제 포스터 연제14 , 10


회장 이성낙 이사장 방동식: , :

1997. 11. 15 제 차 심포지엄7 가톨릭의대 의과학연구원( )

주제 피부과학 연구에서 새로운 연구장비의 활용 발표 연제: , : 7

국외 초청연자 (SID sponsored lecturer) : David A. Norris (Univ. of Colorado)

Warren W. Piette (Univ. of Iowa)

1998. 3. 14 제 차 학술대회8 가톨릭의대 의과학연구원( )

특강연자 : Kazuhiko Takehara (Kanazawa Univ.)

교육강연 연제 자유연제 연제 포스터 연제3 , 15 , 20

심포지엄 연제Wound healing, 5

1998. 9. 24 제 차 심포지엄8

- 138 -

주제 : Bullous dermatoses

특강연자 : Grant J. Anhalt (Johns Hopkins Univ.)

발표 연제: 5

1999. 3. 13 제 차 학술대회9 서울대학교병원 임상의학연구소( )

특강연자 : Alfred T. Lane (Standford Univ.) / 이광훈 연세의대( ) /

Russell P. Hall (Duke Univ.)

자유연제 연제 포스터 연제18 , 21

심포지엄 피부질환 연구를 위한 동물실험기법 연제, 5

제 회 우암학술상 시상 이광훈 연세의대1 : ( )


회장 고재경 이사장 은희철: , :

대한피부연구학회지 년 회 발행4

년부터 년 회에서 회로 발행함1999 2 4

2000. 3. 17 제 차 학술대회10 서울대학교병원 임상의학연구소( )

특강연자: Luis Diaz (North Carolina Univ.)

Irene Leigh (St.Bartholomew's and Royal London School)

Yasuo Kitjma (Gifu Univ.)

자유연제 연제 포스터 연제 심포지엄 자가면역질환 연제18 , 14 , 7

피부생물학 연수교육 강의12

제 회 우암학술상 시상 조광현 서울의대2 : ( )

2001. 3. 17 제 차 학술대회11

특강연자 고베 대학 일본: Masamitsu Ichihashi ( , )

Ralf Paus (Hamburg Uni., Germany)

자유연제 연제 포스터 연제 심포지엄 피부생물학 연수교육 강의16 , 24 , 12

제 회 우암학술상 시상 김도원 경북의대3 : ( )


회장 이정복 이사장 이광훈: , :

2002. 3. 15 제 차 학술대회12 가톨릭대학교 의과대학 의과학 연구원( )

특강연자 : Mark Udey (NIH NCI), Kunihiko Tamaki (Tokyo Uni.)/

Thomas Luger (Westfaelische Wilhelms Uni.),

Setsuya Aiba (Tohoku Uni.)

자유연제 연제 포스터 연제 심포지엄 연제15 , 27 , Dendritic Cell, 7


제 회 우암학술상 시상 김수찬 연세의대4 : )

2003. 3. 28 제 차 학술대회13 강남성모병원 의과학연구원( )

특강연자 미국 의과대학 피부과 교수: Michael J. Detmar, M.D. / Harvard

- 139 -

미국 원장Stephen I. Katz, MD, Ph.D. / NIAMS NIH

독일 대학 피부과 교수Enno Christophers, M.D./ Kiel

자유연제 연제 포스터 연제 심포지엄 연제 피부생물학 연수교육 강의18 , 35 , 6 , 8

제 회 우암학술상 시상 서성준 중앙의대5 : ( )

2004. 3. 26 제 차 학술대회14 서울아산병원 동관 층 대강당( 6 )

특강연자 미국 의과대학 피부과 교수: Thomas S. Kupper, M.D. / Harvard

미국Joost J. Oppenheim, M.D. / NIH Laboratory of Molecular

Immunoregulation

자유연제 연제 포스터연제 연제 심포지엄 연제 피부생물학 연수교육 강의20 , 26 , 6 , 8

제 회 우암학술상 시상 김태윤 가톨릭의대6 : ( )

2005. 3. 25 제 차 학술대회15 서울아산병원 동관 층 대강당( 6 )

특강연자 일본: Akira Ito, Ph.D. / Department of Biochemistry and Molecular

교수Biology, Tokyo University of Pharmacy and Life Science

미국 의대 병리학 교수James Varani, Ph.D. / University of Michigan

자유연제 연제 포스터연제 연제 심포지엄 연제19 , 28 , Extracellular matrix, 7


제 회 우암학술상 시상 이민걸 연세의대6 : ( )

2006. 3. 24 제 차 학술대회16 서울대학교병원 임상의학연구소 층 강당( 1 )

특강연자: 미국Jackie Bickenbach, Ph.D./ Anatomy & Cell Biology,

Dermatology, Molecular Biology, The University of Iowa

일본Emi Nishimura, M.D., Ph.D./ Department of Dermatology and

Creative Research Institute Sousei, Hokkaido University Graduate

School of Medicine

자유연제 연제 포스터연제 연제 심포지엄 연제19 , 62 , Epidermal stem cell 7

연제 피부생물학 연수교육 강의6

제 회 우암학술상 시상 최지호 울산의대8 : ( )


특강연자 미국: Prof. George Cotsarelis, M.D/ Dept of Dermatology, University

of Pennsylvania School of Medicine

일본Prof. Kotaro Yoshimura, M.D./ Department of Plastic Surgery,

University of Tokyo School of Medicine

자유연제 연제19

포스터연제 연제36

심포지엄 연제Stem cell 5

제 회 우암학술상 시상 이증훈9 : 충남의대( )


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특강연자: 프랑스Alain Mauviel Ph.D/ Research Director 2nd class,DR2, INSERM

일본Prof. Hiroshi Shimizu M.D./ Dept of Dermatology Hokkaido

University Graduated School of Medicine

자유연제 연제 포스터연제 연제 연제10 , 40 , 1st KSID-JSID Joint Symposium 6

제 회 우암학술상 시상 이원수 원주의대10 : ( )

2009. 3. 19~ 21 제 차 학술대회19 서울대학교병원 임상의학연구소 층 강당( 1 )

특강연자 : Tan Suat Hoon (National Skin Center, SIN)

Richard Clark (The State Univ. of New York Stony Brook, USA)

John McGrath (King's College, St. Thomas's Hospital, London, GBR)

Dong Youn Lee (Sungkyunkwan Univ., KOR)

Yohanes Widodo (Gadjah Mada Univ., INA)

Amrinder Jit Kanwar (Postgraduate Institute of Medical Education

and Research-Chandigarh, IND)

Li-Fang Wang (National Taiwan Univ. Hospital, TPE)

Phan Hong Hai (Hospital of Dermato-Venereology, Ho Chi Minh

City, VIE)

Zhou Chen (Peking Univ. People's Hospital, CHN)

Belen Dofitas (St. Luke's Medical Center, PHI)

자유연제 연제 포스터연제 연제 연제10 , 40 , Symposium I: Aging 4 ,

연제Symposium II: Animal Models in Dermatologic research 3 ,

제 회 우암학술상 시상 박경찬 서울의대11 : ( )

- 141 -

현 임 원 진년 월 현재(2010 3 )

회 장 단

회 장 문기찬울산의대( )

차 기 회 장 방동식연세의대( )

상 임 이 사　

(2009. 3~2011. 3)　

　　

이 사 장 양준모성균관의대( )

총 무 이 사 정진호서울의대( )

학 술 이 사 김일환고려의대( )

재 무 이 사 최혜 이화의대( )

간 행 이 사 노주 가천의대( )

정 보 이 사 이경호가톨릭의대( )

무임소이사 김창덕충남의대( )

무임소이사 이석종경북의대( )

감 사

(2009. 3~2011. 3)유희준한양의대 김기호동아의대( ), ( )

이 사

임기 년3 　

(2009. 3~2011. 3)　　

이동윤성균관의대 이증훈 충남의대( ), ( ),

안규중건국의대 서성준중앙의대( ), ( ),

조광현서울의대 김규한서울의대( ), ( ),

심우 경희의대 김태윤가톨릭의대( ), ( ),

이준 가톨릭의대( )

임기 년2 　

(2009. 3~2011. 3)　

박경찬서울의대 김문범부산의대( ), ( ),

이민걸연세의대 송해준고려의대( ), ( ),

오승렬숙명여대 박병덕네오팜( ), ( ),

이규석계명의대( )

임기 년1　

(2009. 3~2010. 3)　

윤태진경상의대 원 호전남의대( ), ( ),

박 립순천향의대 박천욱 한림의대( ), ( ),

김도원경북의대 박석돈원광의대( ), ( ),

최지호울산의대( )

당연직이사이사장 상임이사 대한피부과학회 이사장, , ,

태평양 노바티스 한국쉐링 한국스티펠, LG, , ,

- 142 -

학 술 위 원 회

위 원 장 이증훈충남의대( )

간 사 김일환고려의대( )

위 원

박천욱한림의대 이애 동국의대( ), ( ),

박 민가톨릭의대 이주흥 성균관의대( ), ( ),

김성진전남의대 조소연서울의대 보라매병원( ), ( ),

박 립순천향의대 김유찬 아주의대( ), ( ),

최응호연세원주의대 서 준충남의대( ), ( ),

이석종경북의대 김기호동아의대( ), ( ),

김문범부산의대( )

간 행 위 원 회

위 원 장 양준모성균관의대( )

간 사 노주 가천의대( )

부 간 사

위 원

정기양연세의대 송해준고대의대( ), ( ),

김유찬아주의대 이동윤성균관의대( ), ( ),

이원주경북의대( )

정 보 위 원 회

위 원 장 김태윤가톨릭의대( )

간 사 이경호가톨릭의대( )

위 원

조 훈을지의대 이양원건국의대( ), ( ),

김범준중앙의대 김철우한림의대( ), ( ),

김경문가톨릭의대( )

Documents

ProgramandAbstracts - eksideksid.com/pds/files/20______________________.pdf · ProgramandAbstracts 2010.4.2 ... Jeong-Hyun Shin2, SunA Yoon 3, Sang-Joo Park3, ... Tae Kyun Kim, Jin