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. Author manuscript; available in PMC: 2011 Mar 29.
Published in final edited form as: Kidney Int. 2010 May 26;78(4):363–373. doi: 10.1038/ki.2010.137

Figure 5. Targeting ILK activity by small molecule inhibitor QLT0267 abolishes Snail induction and blocks mesenchymal conversion of podocytes.

Figure 5

(a) Small molecule ILK inhibitor QLT0267 selectively inhibited the TGF-β1-induced phosphorylation of GSK-3β, but not Smad3 and p38 MAPK. Podocytes were pretreated with QLT0267 (10 µm) for 0.5 h, followed by incubation with TGF-β1 (2 ng/ml) for different periods of time as indicated. Cell lysates were immunoblotted with various antibodies as indicated. (b) QLT0267 blocked ILK-induced Snail expression in podocytes. Podocytes were infected with Ad.Flag-ILK or Ad.LacZ adenovirus. At 24 h later, cells were treated with different doses of QLT0267 as indicated for additional 24 h. Cell lysates were immunoblotted with specific antibodies against Snail and α-tubulin. (c) Immunofluorescence staining showed that QLT0267 inhibited the desmin, fibronectin, and MMP-9 expression induced by TGF-β1 in podocytes. (d, e) Western blot analyses showed that QLT0267 inhibited the TGF-β1-mediated fibronectin and MMP-9 expression in a dose-dependent manner. Podocytes were treated without or with TGF-β1 (2 ng/ml) in the absence or presence of different doses of QLT0267 as indicated. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GSK-3β, glycogen synthase kinase-3β; ILK, integrin-linked kinase; MAPK, mitogen-activated protein kinase; MMP-9, matrix metalloproteinase-9; TGF-β1, transforming growth factor-β1.