Targeted disruption of TGF-β1/Smad3 signaling protects against renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction
J. Clin. Invest. Misako Sato, et al. 112:1486 doi:10.1172/JCI19270 [Go to this article.]

Figure 5
Smad3-mediated autoinduction of TGF-β1 in cultured renal tubular epithelial cells. (a) Concentration of total TGF-β1 in culture medium of renal tubular epithelial cells from WT and Smad3-null (KO) mice. Results are means ± standard deviation of four to five samples. *P < 0.05 compared with KO. (b) Northern blot of TGF-β1 mRNA in epithelial cells from WT and KO mice in the absence (–) or presence (+) of TGF-β1 (10 ng/ml) for 24 hours. Cells without TGF-β1 were further treated with a neutralizing antibody against TGF-β (20 μg/ml) to exclude any effects of endogenous TGF-β1. The same amount of normal IgG was added to the medium of TGF-β1-treated cells. Results are means ± standard deviation of four samples. *P < 0.01 compared with WT (–), KO (–) or KO (+).