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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Kidney Int. 2015 Feb 4;87(6):1125–1140. doi: 10.1038/ki.2014.406

Figure 5. Dicer1 inactivation in renal FOXD1 lineage results in abnormal podocyte differentiation.

Figure 5

(A) Images of Foxd1−/− glomeruli. The failure of podocytes to mature from epithelial progenitors is readily apparent in Foxd1−/− kidneys by the persistence of cuboidal epithelial morphology. (B) Images showing expression of the mesenchymal transcriptional regulator WT1 in podocytes and the nephrogenic zone during nephrogenesis. Note that in mutant kidneys the expression of WT1 in glomerular cells is markedly reduced at E18.5 and P0 (inset). (C–D) Quantification of positive stained cells of WT1 in the nephrogenic zone (C) and glomeruli (D). (E) Quantification of glomerular fluorescence intensity of WT1. (F) Representative EM images showing lack of mesangium in mutant glomeruli. Note in mutant mice the podocytes show bigger and there is wrinkling and collapse of the capillary loop structure and extensive foot process effacement (arrowheads) (F) Quantification of podocytes diameter. Bar, 25 μm (A,B), 2 μm (E).