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. 2009 Jan 14;4(1):e4194. doi: 10.1371/journal.pone.0004194

Figure 2. Selective depletion of aPKCλ from mouse podocytes results in renal failure.

Figure 2

(A) Double immunofluorescence for aPKCλ (green) and WT1 (magenta) shows that the signals for aPKCλ are below the detectable level in mutant (aPkcλ ΔE5/floxE5;Nphs1-Cre, cKO) podocytes at P0 (arrowheads), whereas the tubular epithelial cells retained aPKCλ in the mutant (arrows). Bar, 20 µm. (B) No significant difference in the gross appearance of mutant (cKO) and control kidneys at P0. (C) One microliter of urine from each mouse at P0 was analyzed along with bovine serum albumin (BSA) by SDS-PAGE and CBB staining. (D) Serum creatinine concentration in mutant mice compared with controls. Triangles, controls carrying the Nphs1-Cre transgene; diamonds, mutants; bars, medians. The p values were determined by the two-tailed Mann–Whitney U-test. (E) Mutant mice (cKO) show growth retardation by the age of 4 weeks. Values are mean±S.E.M. (F) Kaplan–Meier survival curve for mutant (cKO) and control mice.