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Journal of Lipid Research, Vol. 46, 1712-1720, August 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Eicosapentaenoic acid inhibits UV-induced MMP-1 expression in human dermal fibroblasts

Hyeon Ho Kim^a,b,c, Chung Min Shin^a,b,c, Chi-Hyun Park^a,b,c, Kyu Han Kim^a,b,c, Kwang Hyun Cho^a,b,c, Hee Chul Eun^a,b,c and Jin Ho Chung^1,a,b,c

^a Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea
^b Laboratory of Cutaneous Aging Research, Clinical Research Institutes, Seoul National University Hospital, Seoul, Korea
^c Institute of Dermatological Science, Seoul National University, Seoul, Korea

Published, JLR Papers in Press, June 1, 2005. DOI 10.1194/jlr.M500105-JLR200

¹ To whom correspondence should be addressed. e-mail: jhchung{at}snu.ac.kr

Ultraviolet (UV) irradiation regulates UV-responsive genes, including matrix metalloproteinases (MMPs). Moreover, UV-induced MMPs cause connective tissue damage and the skin to become wrinkled and aged. Here, we investigated the effect of eicosapentaenoic acid (EPA), a dietary -3 fatty acid, on UV-induced MMP-1 expression in human dermal fibroblasts (HDFs). We found that UV radiation increases MMP-1 expression and that this is mediated by p44 and p42 MAP kinase (ERK) and Jun-N-terminal kinase (JNK) activation but not by p38 activation. Pretreatment of HDFs with EPA inhibited UV-induced MMP-1 expression in a dose-dependent manner and also inhibited the UV-induced activation of ERK and JNK by inhibiting ERK kinase (MEK1) and SAPK/ERK kinase 1 (SEK1) activation, respectively. Moreover, inhibition of ERK and JNK by EPA resulted in the decrease of c-Fos expression and c-Jun phosphorylation/expression induced by UV, respectively, which led to the inhibition of UV-induced activator protein-1 DNA binding activity. This inhibitory effect of EPA on MMP-1 was not mediated by an antioxidant effect. We also found that EPA inhibited 12-O-tetradecanoylphorbol-13-acetate- or tumor necrosis factor--induced MMP-1 expression in HDFs and UV-induced MMP-1 expression in HaCaT cells.

In conclusion, our results demonstrate that EPA can inhibit UV-induced MMP-1 expression by inhibiting the MEK1/ERK/c-Fos and SEK1/JNK/c-Jun pathways. Therefore, EPA is a potential agent for the prevention and treatment of skin aging.

Abbreviations: AA, arachidonic acid; AP-1, activator protein-1; COX-2, cyclooxygenase-2; DCF-DA, 2'-7'-dichlorofluorescein diacetate; DHA, docosahexaenoic acid; EMSA, electrophoretic mobility shift assay; EPA, eicosapentaenoic acid; ERK, p44 and p42 MAP kinase; JNK, Jun-N-terminal kinase; HDF, human dermal fibroblast; LA, linolenic acid; MAPK, mitogen-activated protein kinase; MEK1, MAP or ERK kinase; MMP-1, matrix metalloproteinase-1; NAC, N-acetyl cysteine; OA, oleic acid; PGE, prostaglandin E; PMSF, phenylmethylsulfonyl fluoride; ROS, reactive oxygen species; SEK, SAPK/ERK kinase; TNF-, tumor necrosis factor-; TPA, 12-O-tetradecanoylphorbol-13-acetate; UV, ultraviolet

Supplementary key words ultraviolet radiation • matrix metalloproteinase-1 • polyunsaturated fatty acid

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