Transforming growth factor-β1 induces collagen synthesis and accumulation via p38 mitogen-activated protein kinase (MAPK) pathway in cultured L6E9 myoblasts

被引：56

作者：

Rodríguez-Barbero, A

Obreo, J

Yuste, L

Montero, JC

Rodríguez-Peña, A

Pandiella, A

Bernabéu, C

López-Novoa, JM ^{[1
]}

机构：

[1] Univ Salamanca, Dept Fisiol & Farmacol, Inst Reina Sofia Invest Nefrol, Salamanca, Spain

[2] Univ Salamanca, Consejo Super Invest Cient, Inst Microbiol & Bioquim, Edificio Dept, Salamanca 37007, Spain

[3] CSIC, Ctr Invest Biol, Madrid 28006, Spain

来源：

FEBS LETTERS | 2002年 / 513卷 / 2-3期

关键词：

extracellular matrix; fibrosis; signaling; transforming growth factor-beta 1;

D O I：

10.1016/S0014-5793(02)02337-2

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：

Transforming growth factor-beta (TGF-beta) plays a pivotal role in the extracellular matrix accumulation observed in chronic progressive tissue fibrosis, but the intracellular signaling mechanism by which TGF-beta stimulates this process remains poorly understood. We examined whether mitogen-activated protein kinase (MAPK) routes were involved in TGFbeta1-induced collagen expression in L6E9 myoblasts. TGF-beta1 induced p38 and extracellular signal-regulated kinase (ERK) 1/2 phosphorylation whereas no effect on Jun N-terminal kinase phosphorylation was observed. Biochemical blockade of p38 but not of the ERK MAPK pathway abolished TGF-beta1-induced alpha(2)(I) collagen mRNA expression and accumulation. These data indicate that TGF-beta1-induced p38 activation is involved in TGF-beta1-stimulated collagen synthesis. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：282 / 288

页数：7

共 31 条

[1] Induction of apoptosis by DPC4, a transcriptional factor regulated by transforming growth factor-beta through stress-activated protein kinase c-Jun N-terminal kinase (SAPK/JNK) signaling pathway [J].