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. 2011 Aug 18;17(11-12):1275–1284. doi: 10.2119/molmed.2011.00125

Figure 1.

Figure 1

Deficits in renal differentiation and Wt1 expression in embryonic kidneys from Ahr−/− mice. Kidneys were harvested from mouse embryos at GD:14 and fixed in situ for morphological examination as described. (A) Renal blastema in the proliferation zone was less condensed in developing kidneys from Ahr knockout embryos relative to wild-type counterparts (compare panels 1 and 2). Magnification in both panels was 289X. Similar findings were made in 10 mice from multiple litters. (B) Morphometric analyses of kidney sections showed decreased numbers of glomeruli and tubulo-epithelial structures (P < 0.05), despite equal numbers of comma and S-shaped bodies in Ahr knockout compared with wild-type mice. Data are presented as the average number of structures ± SD for multiple sections. Measurements were taken from serial sections from 6 to 8 embryonic kidneys isolated from three or more dams. The values shown represent the composite of serial sections with variance expressed as the difference between values for each kidney per mouse strain. (C) PCR analyses of Wt1 splice variants in embryonic kidneys of Ahr −/− compared with wild-type mice. (D) PCR analysis of various markers of renal cell differentiation (Igf-1 rec, Wnt4 and E-cadherin) in embryonic kidneys from Ahr−/− and Ahr+/+ mice. (E) Western blot analysis of Ahr and Wt1 in kidneys of Ahr−/− and Ahr+/+ mice. One representative experiment out of two is shown. Equal protein loadings were confirmed based on the signal obtained with the same antibody for a nonspecific band (80 kDa).