p38 MAPK mediates the regulation of α1(I) procollagen mRNA levels by TNF-α and TGF-β in a cell line of rat hepatic stellate cells

被引：78
|
作者：
Varela-Rey, M
Montiel-Duarte, C
Osés-Prieto, JA
López-Zabalza, MJ
Jaffrèzou, JP
Rojkind, M
Iraburu, MJ
机构：
[1] Univ Navarra, Dept Biochem, Pamplona 31008, Spain
[2] INSERM, E9910, Inst Claudius Regaud, F-31052 Toulouse, France
[3] Walter Reed Army Med Ctr, Dept Clin Invest, Washington, DC 20307 USA
来源：
FEBS LETTERS | 2002年 / 528卷 / 1-3期
关键词：
p38; MAPK; TNF-alpha; TGF-beta; hepatic stellate cells; A-SMase; alpha 1(I) procollagen;
D O I：
10.1016/S0014-5793(02)03276-3
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The role of members of the mitogen-activated protein kinase (MAPK) family on tumor necrosis factor alpha (TNF-alpha)mediated down-regulation of col1a1 gene was studied. TNF-alpha increased extracellular-regulated kinase and Jun-N-terminal kinase phosphorylation, but these effects were not related to its inhibitory effect on alpha1(I) procollagen (col1a1) mRNA levels. Phosphorylation of p38 MAPK was decreased in response to TNT-alpha and the specific p38 MAPK inhibitor SB203580 mimicked the effect of TNF-alpha on col1a1 mRNA levels. Transforming growth factor beta (TGF-beta) increased p38 MAPK phosphorylation and SB203580 prevented the induction of col1a1 mRKA levels by TGF-beta. These results suggest that p38 MAPK plays an important role in regulating the expression of col1a1 in hepatic stellate cells in response to cytokines. (C) 2002 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
引用
收藏
页码：133 / 138
页数：6
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