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. 2020 Aug 28;11:4320. doi: 10.1038/s41467-020-18104-5

Fig. 3. Expression of CFTR and cell proliferation in Pkd1−/− kidneys depends on TMEM16A.

Fig. 3

a Enhanced tubular epithelial expression of CFTR and TMEM16A in kidneys from Pkd1−/− mice that was abolished in kidneys from Pkd1−/−/T16a−/− double-knockout mice. Both, CFTR and TMEM16A were colocalized in the apical membrane of the cyst epithelium. (blue; DAPI). bd Expression of TMEM16A (#P < 0.0001) and CFTR (#P < 0.0001) were enhanced (n = 25 independent images over 5 animals) in Pkd1−/− mice. Significant colocalization of TMEM16A and CFTR was detected (#P = 0.0006) using colocalization finder algorithm (ImageJ, V.1.49 by Laummonerie and Mutterer). Expression of CFTR (§P = 0.0006) and TMEM16A (§P = 0.0006), as well as colocalization (§P = 0.0001) were lower in Pkd1−/−/T16a−/− mice. e, f ki-67 staining was enhanced in tubular epithelial cells from Pkd1+/+ (#P < 0.0001) animals but was lower in cells from Pkd1−/−/T16a−/− kidneys (§P < 0.0001) (n = 25 independent images from 5 animals). Mean and error bars indicating ±SEM. one-way ANOVA and Tukey’s post-hoc test comparing Pkd1+/+ with Pkd1−/− and Pkd1−/− with Pkd1−/−/T16a−/−, respectively. Source data are provided as a Source Data file.