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Fig. 6 | BMC Developmental Biology

Fig. 6

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

Fig. 6

Wnt11 deficiency reduces cell proliferation and increases apoptosis in the kidney. Kidneys were prepared from WT and Wnt11 −/− mice and processed for immunohistochemistry. The sections were stained with phospho-Histone-3 (P-H3) antibodies, LTL and DAPI for cell proliferation and TUNEL for apoptosis. ad Representative cell proliferation images obtained by confocal microscopy (a, c). Corresponding brightfield images are also shown (b, d). Wnt11 −/− reduced cell proliferation in the nephron-forming cortex of C57Bl6 mice, as judged by the presence of P-H3 staining (in red) mainly in the non-LTL+ cells (green) (compare cd with ab, several proliferating cells marked with arrows). eh Cells in the developing cortex region underwent increased apoptosis in the absence of Wnt11 signaling, as indicated by the TUNEL assay (compare gh with ef, several apoptotic cells marked with arrows). i Quantification of TUNEL data (percentage of apoptotic cells in Wnt11 −/− and control samples) and P-H3 data (percentage of proliferating cells in Wnt11 −/− and control samples). Bars: 50 μm

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