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 6
Epithelial-mesenchymal transition and TGF-β1 upregulation in an environment of mechanical stretch. (a–d) Dual immunofluorescence of E-cadherin (green) and α-SMA (red) in renal tubular epithelial cells derived from WT (a and b) and Smad3-null (KO) mice (c and d) stretched for 24 hours in the absence (a and c) or presence (b and d) of neutralizing anti–TGF-β1 (20 μg/ml). Scale bars: 20 μm. (e) Northern blot of Snail mRNA in the epithelial cells either stretched for 24 hours or nonstretched, in the absence or presence of neutralizing anti–TGF-β1. Similar results were obtained from additional two experiments. (f) Northern blot of TGF-β1 mRNA in primary culture of the epithelial cells either stretched for 24 hours or nonstretched, in the absence or presence of a neutralizing anti–TGF-β1 antibody. Results are means ± standard deviation of five samples. *P < 0.01 compared with other experimental groups. (g) Total TGF-β1 concentration in culture medium of epithelial cells either stretched or nonstretched. Results are means ± standard deviation of five samples. *P < 0.05 compared with nonstretched counterparts.