| Literature DB >> 12297293 |
M Varela-Rey1, C Montiel-Duarte, J A Osés-Prieto, M J López-Zabalza, J P Jaffrèzou, M Rojkind, M J Iraburu.
Abstract
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 TNF-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 mRNA 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.Entities:
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Year: 2002 PMID： 12297293 DOI： 10.1016/s0014-5793(02)03276-3
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124