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 cells11The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense of the US.

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Title: 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 cells11The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense of the US.
Authors: Varela-Rey, M.1, Montiel-Duarte, C.1, Osés-Prieto, J.A.1, López-Zabalza, M.J.1, Jaffrèzou, J.P.2, Rojkind, M.3, Iraburu, M.J.1 miraburu@unav.es
Source: FEBS Letters. Sep2002, Vol. 528 Issue 1-3, p133. 6p.
Subjects: Tumor necrosis factors, Transforming growth factors-beta, Phosphorylation
Abstract: The role of members of the mitogen-activated protein kinase (MAPK) family on tumor necrosis factor α (TNF-α)-mediated down-regulation of col1a1 gene was studied. TNF-α increased extracellular-regulated kinase and Jun-N-terminal kinase phosphorylation, but these effects were not related to its inhibitory effect on α1(I) procollagen (col1a1) mRNA levels. Phosphorylation of p38 MAPK was decreased in response to TNF-α, and the specific p38 MAPK inhibitor SB203580 mimicked the effect of TNF-α on col1a1 mRNA levels. Transforming growth factor β (TGF-β) increased p38 MAPK phosphorylation and SB203580 prevented the induction of col1a1 mRNA levels by TGF-β. These results suggest that p38 MAPK plays an important role in regulating the expression of col1a1 in hepatic stellate cells in response to cytokines. [Copyright &y& Elsevier]
Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: 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<superscript>1</superscript><FN ID="FN1"><NO>1</NO>The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense of the US.</FN>
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  Data: <searchLink fieldCode="JN" term="%22FEBS+Letters%22">FEBS Letters</searchLink>. Sep2002, Vol. 528 Issue 1-3, p133. 6p.
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  Data: The role of members of the mitogen-activated protein kinase (MAPK) family on tumor necrosis factor α (TNF-α)-mediated down-regulation of col1a1 gene was studied. TNF-α increased extracellular-regulated kinase and Jun-N-terminal kinase phosphorylation, but these effects were not related to its inhibitory effect on α1(I) procollagen (col1a1) mRNA levels. Phosphorylation of p38 MAPK was decreased in response to TNF-α, and the specific p38 MAPK inhibitor SB203580 mimicked the effect of TNF-α on col1a1 mRNA levels. Transforming growth factor β (TGF-β) increased p38 MAPK phosphorylation and SB203580 prevented the induction of col1a1 mRNA levels by TGF-β. These results suggest that p38 MAPK plays an important role in regulating the expression of col1a1 in hepatic stellate cells in response to cytokines. [Copyright &y& Elsevier]
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  Data: <i>Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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