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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 6. Dicer1 inactivation in renal stromal progenitors results in abnormal vascular patterning.

Figure 6

(A) Images of CD31+ endothelium of the developing kidney. Note that at E15.5 many endothelial cells of the PTCs are not connected to one another in mutant kidneys (arrowheads) whereas in controls they already form a connected vasculature. In P0 kidney cortex, mutant capillaries are now connected but show very wide capillaries with enhanced branching (arrow). These differences were less apparent in the medulla. (B–D) Quantification of number of unconnected vessels (B), number of branching points per unit area (C) and diameter of CD31+ vessels (D). (E) Representative EM images of peritubular capillaries showing abnormal dilatation, and pericytes containing abnormal vacuoles in mutant kidneys (arrowheads). L, capillary lumen; Pc, pericytes; EC, endothelial cells; Fb, fibroblasts. (F) PAS stained sections showing absent or attenuated mesangium (arrow) in some mutant glomeruli at P0. (G) Quantification of number of glomeruli lacking mesangium. Glomeruli which lacked a mesangium showed a single lumen capillary surrounded by immature podocytes. (N.D., not detected). (H–I) Quantification of glomerular maturity index at P0 (3 > 2 > 1). Mature glomeruli were decreased both in outer (H) and inner cortex (I) in mutant kidneys. (J–K) Images of VSMCs (J; PAS stain, K; αSMA+ expression) in control and mutant kidneys showing a reduction in number of layers of smooth muscle. (L) Quantification of thickness of αSMA+ VSMCs. Bar, 25 μm (A, F, J, K). 2 μm (E). *P < 0.05, **P < 0.01, n = 3–5/group.