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Fig. 5 | BMC Developmental Biology

Fig. 5

From: Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis

Fig. 5

Wnt11 deficiency leads to the heterogeneity in cell numbers in specific tubular segmental regions. Kidneys from WT and Wnt11 −/− mice were prepared, sectioned and processed for immunohistochemistry with markers lectin LTL for the proximal tubule, in green, AQP2 for the collecting ducts, in red, and DAPI, for nuclei, in blue. ah The staining of the cross-sections of the tubules at corresponding spatial location emphasizes that Wnt11 deficiency leads to enlarged luminal diameter of the proximal tubules and collecting ducts in the kidney of NB (compare b, f with a, e, circled area) and adult mice (compare d, h with c, g, circled area). Note that the brush border, depicted with the LTL lectin marker, is more prominent and also abnormally organized in the proximal tubular cells of the Wnt11 −/− kidneys relative to the controls (compare b with a, arrows). i, j Histograms showing estimated percentages of the tubules having the given numbers of cells per cross-section. The Wnt11 deficient proximal and collecting ducts had increased percentages of tubules with an abnormally high cell number per cross-section relative to the values obtained from WT kidneys. Each colour indicates the number of cells/tubule cross-section (from 3 to 9–10 cells). Note that this phenotype was more obvious in the kidneys of the adult Wnt11-deficient mice. Bars: 25 μm

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