Transforming growth factor-β1-induced activation of the Raf-MEK-MAPK signaling pathway in rat lung fibroblasts via a PKC-dependent mechanism

被引：72

作者：

Axmann, A ^{[1
]}

Seidel, D ^{[1
]}

Reimann, T ^{[1
]}

Hempel, U ^{[1
]}

Wenzel, KW ^{[1
]}

机构：

[1] Tech Univ Dresden, Med Fac Carl Gustav Carus, Inst Physiol Chem, D-01109 Dresden, Germany

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 249卷 / 02期

关键词：

D O I：

10.1006/bbrc.1998.9188

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：

In fibroblasts transforming growth factor-beta 1 (TGF-beta 1) regulates cell proliferation and turnover of macromolecular components of the extracellular matrix. Here, intracellular signaling events in growth-inhibited embryonic rat lung fibroblasts (RFL-6) upon stimulation with TGF-beta 1 were investigated. TGF-beta 1 rapidly induced the activation of c-Raf-1, MEK-1, and MAPK p42 and p44. The activation of this pathway by TGF-beta 1 did not depend on autocrine platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF). Inhibition of the binding of growth factors to their tyrosine kinase receptors did not affect MAPK activation by TGF-beta 1. Ras activation by TGF-beta 1 was significantly lower compared to the activation by PDGF or bFGF. The intracellular transduction of the TGF-beta 1 signal was completely suppressed by depletion or inhibition of protein kinase C (PKC). It is shown that calcium-dependent isoforms of PKC are required for MAPK activation by TGF-beta 1. (C) 1998 Academic Press.

引用

页码：456 / 460

页数：5

共 37 条

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