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. 2019 Oct 21;317(6):F1649–F1655. doi: 10.1152/ajprenal.00395.2019

Fig. 1.

Fig. 1.

A: schema of CRISPR-induced insertion in exon 2 of the P2X receptor (P2rx7) gene leading to a frameshift mutation. B: Western blot demonstrating P2X7 protein expression in total kidney samples of polycystic kidney (PCK) rat littermates with different genotypes. GAPDH expression was used as a loading control. C: P2X4 abundance in kidneys was not affected in heterozygous or knockout rats. D: body weight progression with aging (n = 6–14). E: 24-h urinary sodium excretion measured in young and adult rats (n = 11–21). F: glomerular filtration rate (GFR) measured in 24-wk-old Sprague-Dawley (SD), PCK.P2rx7+/+, and PCK.P2rx7−/− rats (n = 5–7). PCK.P2rx7+/+, PCK rats with intact P2rx7; PCK.P2rx7−/−, PCK rats with P2rx7−/− knockout; PCK.P2rx7+/−, PCK rats heterozygous for P2rx7−/−. Plasma FITC-inulin clearance in conscious animals was measured after a bolus intravenous administration and GFR was calculated in the 2-compartment model. *P < 0.05 vs. the SD group.