Smad3 mediates TGF-beta1-induced collagen gel contraction by human lung fibroblasts

Tetsu Kobayashi, Xiangde Liu, Fu-Qiang Wen, Tadashi Kohyama, Lei Shen, Xing Qi Wang, Mitsuyoshi Hashimoto, Lijun Mao, Shinsaku Togo, Shin Kawasaki, Hisatoshi Sugiura, Koichiro Kamio, Stephen I Rennard
Biochemical and Biophysical Research Communications 2006 January 6, 339 (1): 290-5
Transforming growth factor-beta1 (TGF-beta1) is a key mediator in tissue repair and fibrosis. Using small interference RNA (siRNA), the role of Smad2 and Smad3 in TGF-beta stimulation of human lung fibroblast contraction of collagenous matrix and induction of alpha-SMA and the role of alpha-SMA in contraction were assessed. HFL-1 cells were transfected with Smad2, Smad3 or control-siRNA, and cultured in floating Type I collagen gels +/- -TGF-beta1. TGF-beta1 augmented gel contraction in Smad2-siRNA- and control-siRNA-treated cells, but had no effect in Smad3-siRNA-treated cells. Similarly, TGF-beta1 upregulated alpha-SMA in Smad2-siRNA- and control-siRNA-treated cells, but had no effect on Smad3-siRNA-treated cells. Alpha-SMA-siRNA-treated cells did not contact the collagen gels with or without TGF-beta1, suggesting alpha-SMA is required for gel contraction. Thus, Smad3 mediates TGF-beta1-induced contraction and alpha-SMA induction in human lung fibroblasts. Smad3, therefore, could be a target for blocking contraction of human fibrotic tissue induced by TGF-beta1.

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