Figure 3.

Crb2 depletion in podocytes results in altered expression of slit diaphragm proteins and activation of injury pathways. (A and B) Representative immunofluorescence analysis of glomeruli from Crb2 ^flox/flox and Crb2 ^podKO 8-week-old mice. (A) In contrast to Crb2 ^flox/flox littermate controls that showed strong expression and colocalization of slit diaphragm proteins Nephrin (red) and Podocin (green), (B) slit diaphragm protein expression was decreased in Crb2 ^podKO. Boxes show details in higher magnifications below the merged images. Scale bars: 10 µm. (C) Relative gene expression (normalized to Crb2 ^flox/flox littermates) of renal injury and inflammation markers of 1-, 5-, and ≥8-week-old animals (n=3–5 animals per group). The tested markers for inflammation (Ccl2) and tubulointerstitial (Havcr1, Lcn2, and Serpine1) and glomerular injury (Tagln1) remained unchanged within the first week and changed significantly after 5 weeks. During the next 3 weeks (8 weeks), all injury markers (particularly, Ccl2, Havcr1, and Lcn2) were strongly upregulated. Unpaired two-tailed t test. *P=0.05; **P=0.01; ***P<0.001.