Involvement of ERK and p38 MAP kinase in AAPH-induced COX-2 expression in HaCaT cells
- Authors
- Cui, Yong; Kim, Dong-Seok; Park, Seo-Hyoung; Yoon, Jin-A; Kim, Soon-Kyum; Kwon, Sun-Bang; Park, Kyoung-Chan
- Issue Date
- Apr-2004
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- ERK; p38 MAPK; AAPH; COX-2; inflammation
- Citation
- CHEMISTRY AND PHYSICS OF LIPIDS, v.129, no.1, pp 43 - 52
- Pages
- 10
- Journal Title
- CHEMISTRY AND PHYSICS OF LIPIDS
- Volume
- 129
- Number
- 1
- Start Page
- 43
- End Page
- 52
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/66858
- DOI
- 10.1016/j.chemphyslip.2003.11.004
- ISSN
- 0009-3084
1873-2941
- Abstract
- Cyclooxygenase-2 (COX-2) appears to play an important role in inflammation and carcinogenesis, and 2,2'-azobis (2-amidino-propane) dihydrochloride (AAPH) is a hydrophilic azo compound known to generate free radicals. Because reactive oxygen species (ROS) are known to elevate COX-2 expression, we evaluated the effect of AAPH on the expression of COX-2 in a human keratinocyte cell line, HaCaT When cells were exposed to AAPH, marked COX-2 induction was observed. To clarify the signaling mechanism involved, we next investigated the effects of AAPH upon three major subfamilies of the mitogen-activated protein kinases (MAPKs). AAPH caused an increase in the phosphorylation of extracellular signal-regulated kinase (ERK), p38 and c-Jun NH2-terminal kinase (JNK). Furthermore, we found that PD98059, an ERK pathway inhibitor, and S13203580, a p38 MAPK inhibitor, diminished AAPH-induced COX-2 expression and PGE(2) production, whereas JNK inhibitor did not suppress COX-2 expression or PGE, production by AAPH. These findings suggest that the ERK and p38 MAPK pathways, but not the JNK pathway, are involved in AAPH-induced inflammatory progression. In addition, we found that both the water-soluble Vitamin E derivative. Trolox, and the green tea constituent, (-)-epigallocatechin gallate (EGCG), diminished AAPH-induced COX-2 expression and p38 activation. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
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