Glutathione redox regulates TGF-β-induced fibrogenic effects through Smad3 activation

被引：21

作者：

Ono, Akihiro ^{[1
]}

Utsugi, Mitsuyoshi ^{[1
]}

Masubuchi, Ken ^{[1
]}

Ishizuka, Tamotsu ^{[1
]}

Kawata, Tadayoshi ^{[1
]}

Shimizu, Yasuo ^{[1
]}

Hisada, Takeshi ^{[1
]}

Hamuro, Junji ^{[2
]}

Mori, Masatomo ^{[1
]}

Dobashi, Kunio ^{[3
]}

机构：

[1] Gunma Univ, Grad Sch Med, Dept Med & Mol Sci, Maebashi, Gunma 3718511, Japan

[2] Keio Univ, Sch Med, Dept Microbiol & Immunol, Tokyo, Japan

[3] Gunma Univ, Fac Med, Sch Hlth Sci, Maebashi, Gunma 3718511, Japan

来源：

FEBS LETTERS | 2009年 / 583卷 / 02期

关键词：

Glutathione redox; Transforming growth factor-beta; Smad; Fibrogenic effect; Human lung fibroblast; Bronchial smooth muscle cell; TISSUE GROWTH-FACTOR; SMOOTH-MUSCLE CELLS; TRANSFORMING GROWTH-FACTOR-BETA-1; EXTRACELLULAR-MATRIX; EXPRESSION; BINDING; RANTES; MODEL; P38;

D O I：

10.1016/j.febslet.2008.12.021

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 fibrogenic action involved in theinduction of connective tissue growth factor (CTGF), extracellular matrix and fibroblast transformation. Smad3 mediates TGF-beta signaling related to the fibrotic response. In human lung fibroblasts or bronchial smooth muscle cells, we demonstrated that an increase in the intracellular glutathione level suppressed TGF-beta 1-induced phosphorylation of Smad3, while inhibiting TGF-beta 1-induced expressions of CTGF, collagen type1, fibronectin and transformation into myofibroblasts, which are characterized by the expression of alpha-smooth muscle actin. These data indicate that the intracellular glutathione redox status regulates TGF-beta-induced fibrogenic effects through Smad3 activation. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：357 / 362

页数：6

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