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. 2011 Apr;178(4):1899–1912. doi: 10.1016/j.ajpath.2010.12.049

Figure 5.

Figure 5

Effect of PTK/ZK on receptor tyrosine kinase signaling, glomerular volume, and mesangial cells during nephritis. PTK/ZK administered i.p. during nephritis led to the inhibition of glomerular expression and phosphorylation of VEGFR2 (A and B, n = 4) and PDGFRβ (D and E, n = 4) but not VEGFR1 (D and F, n = 4). Glomerular expression and activity of PKB was partially inhibited as a result of PTK/ZK treatment (A and C, n = 4). PTK/ZK transiently prevented nephritis-induced glomerular hypertrophy (G, n = 3–4). Treatment with PTK/ZK resulted in the decrease of α-SMA and tensin expression, but the compound did not influence the expression of Thy1.1, fibronectin, and collagen type IV (H). Expression of these proteins was normalized to β-actin and quantified with ImageJ software (I–M, n = 4). *P < 0.05, **P < 0.01, ***P < 0.0001.