Skip to main content
. 2010 Sep;177(3):1065–1071. doi: 10.2353/ajpath.2010.090923

Figure 1.

Figure 1

TGF-β1-induced Smad3 acetylation (A-Smad3) and phosphorylation (p-Smad3) in rat renal NRK49F fibroblasts. A: Immunoprecipitation (IP)/Western blotting (WB) shows a time course of TGF-β1 (4 ng/ml)-induced Smad3 acetylation and phosphorylation, and a TGF-β1 dose-response at the 60-minute time point. B: IP/WB analysis of the effect of Resveratrol (Res) on TGF-β1-induced Smad3 acetylation and phosphorylation. The addition of 10 μmol/L Res to NRK49F cells suppressed Smad3 acetylation at three hours but not one hour, while the addition of 5 μmol/L Res suppressed Smad3 acetylation at 3 hours in NRK52E cells. C: WB in top panel shows that SIRT1 siRNA but not control siRNA knocks down SIRT1 protein levels in NRK49F cells. IP/WB analysis in bottom panel shows that TGF-β1-induced Smad3 acetylation at three hours is suppressed by Res, but this suppression is lost in the presence of SIRT1 siRNA. D: Real-time RT-PCR analysis of mRNA levels in NRK49F cells 24 hours after TGF-β1 stimulation. The addition of 10 μmol/L Res suppressed TGF-β1-induced up-regulation of α-SMA, collagen IV, and fibronectin, and this effect of Res was prevented by SIRT1 siRNA but not control siRNA. Data are mean ± SD. *P < 0.05.