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全反式维甲酸抑制TGF-β1诱导的大鼠肾系膜细胞纤维连接蛋白表达及Smad 2,3,4核转位

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Purpose To investigate the effects of all-trans retinoic acid (atRA) on transforming growth factor-β1 (TGF-β1)-induced fibronectin expression and Smad pathway activation in cultured rat renal mesangial cells. Methods Fibronectin expression, phosphorylation of Smad 2, nuclear translocation of phosphor-Smad 2, total Smad 2/3, Smad 4 induced by TGF-β1 in the presence or absence of atRA in the mesangial cells were analysed by Western blotting. Results atRA inhibited fibronectin expression induced by TGF-β1. atRA did not affect TGF-β1-induced phosphorylation of Smad 2, however, atRA attenuated TGF-β1-induced nuclear translocation of phospho-Smad 2, Smad 2/3, and Smad 4. Conclusions The in Vitro anti-fibrotic actions of atRA are presumably due to a decreased nuclear translocation of phospho-Smad 2, Smad 2/3 and Smad 4 in mesangial cells stimulated with TGF-β1.

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Purpose To investigate the effects of all-trans retinoic acid (atRA) on transforming growth factor-β1 (TGF-β1)-induced fibronectin expression and Smad pathway activation in cultured rat renal mesangial cells. Methods Fibronectin expression, phosphorylation of Smad 2, nuclear translocation of phosphor-Smad 2, total Smad 2/3, Smad 4 induced by TGF-β1 in the presence or absence of atRA in the mesangial cells were analysed by Western blotting. Results atRA inhibited fibronectin expression induced by TGF-β1. atRA did not affect TGF-β1-induced phosphorylation of Smad 2, however, atRA attenuated TGF-β1-induced nuclear translocation of phospho-Smad 2, Smad 2/3, and Smad 4. Conclusions The in Vitro anti-fibrotic actions of atRA are presumably due to a decreased nuclear translocation of phospho-Smad 2, Smad 2/3 and Smad 4 in mesangial cells stimulated with TGF-β1.

Keywords

SMADFibronectinPhosphorylationTransforming growth factorSmad2 ProteinChemistryCancer researchMesangial cell

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