Skip to main content
. 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 8. Targeting ILK in vivo ameliorates the ADR-mediated glomerular injury and preserves nephrin expression.

Figure 8

(a–d) Whole-glomerular lysates were analyzed by western blotting using specific antibodies against MMP-9, α-SMA, nephrin, and GAPDH. (a) Representative western blots. (b–d) Quantitative data on MMP-9 (b), α-SMA (c), and nephrin (d) are presented as mean ± s.e.m. (n = 6). *P < 0.05 versus normal controls, †P < 0.05 versus ADR alone controls. (e) Confocal immunofluorescence microscopy showed the distribution of nephrin and podocalyxin in mouse glomeruli at 7 days after ADR injection. QLT0267 largely preserved nephrin expression after ADR. (f) Semiquantitative evaluation on nephrin loss (injury score) in the glomeruli among different groups. *P < 0.05 versus normal controls, †P < 0.05 versus ADR alone (n = 6). ADR, adriamycin; α-SMA, α-smooth muscle actin; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; ILK, integrin-linked kinase; MMP-9, matrix metalloproteinase-9.