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 4
Smad3-mediated EMT in cultured renal tubular epithelial cells. (a–d) Phase-contrast microscopy of epithelial cells from WT (a and b) and Smad3-null (KO) (c and d) mice in the absence (a and c) or presence (b and d) of TGF-β1 (10 ng/ml) for 24 hours. Scale bars: 100 μm. (e–h) Dual immunofluorescence of E-cadherin (green) and α-SMA (red) in epithelial cells from WT (e and f) and KO (g and h) mice in the absence (e and g) or presence (f and h) of TGF-β1 (10 ng/ml) for 24 hours. Scale bars: 20 μm. (i) Immunoblot of E-cadherin (E-cad) and α-SMA with extracted protein from epithelial cells of WT and KO mice in the absence (–) or presence (+) of TGF-β1 (10 ng/ml) for 24 hours. (j) Northern blot of Snail mRNA in the epithelial cells from WT and KO mice in the absence (–) or presence (+) of TGF-β1 (10 ng/ml) for 8 hours. Similar results were obtained from three additional experiments.