| Literature DB >> 19101551 |
Akihiro Ono1, Mitsuyoshi Utsugi, Ken Masubuchi, Tamotsu Ishizuka, Tadayoshi Kawata, Yasuo Shimizu, Takeshi Hisada, Junji Hamuro, Masatomo Mori, Kunio Dobashi.
Abstract
Transforming growth factor-beta (TGF-beta) plays a pivotal role in the fibrogenic action involved in the induction 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-beta1-induced phosphorylation of Smad3, while inhibiting TGF-beta1-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.Entities:
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Year: 2008 PMID： 19101551 DOI： 10.1016/j.febslet.2008.12.021
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124