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. 2015 May 12;27(1):144–157. doi: 10.1681/ASN.2014111109

Figure 1.

Figure 1.

Whole-body p53 deletion promotes the progression of renal dysfunction in X-linked AS mouse model. (A) Glomeruli were isolated from WT or AS mice in early (10 weeks) or late (21 weeks) stage of AS. Proteins were extracted from glomeruli and p53 protein was analyzed by immunoblotting. Actin was used as loading control. Relative amount of p53 was quantified and normalized to actin (mean±SEM, n=3). **P<0.01 versus WT. (B) Urine samples were obtained from 12-week-old mice of each genotype, and urinary albumin score was measured. U-Albumin scores were normalized with urine creatinine score (mean±SEM, n=4–10). (C) Urine samples were collected at 6, 9, 12, 15, 18, 21, and 24 weeks, and protein concentration was measured. Proteinuria score was calculated based on the urine protein concentration and urine creatinine score (mean±SEM, n=3–8). Measuring proteinuria score of p53−/− AS group was terminated at 15 weeks due to the death of all mice in this group. (D) BUN score of p53+/+ AS and p53−/− AS mice was measured at 6 and 12 weeks (mean±SEM, n=5–7). (E) Survival rate of p53+/+, +/−, −/− AS mice was measured and analyzed by Kaplan–Meier method. Log-rank test was used for statistical analysis (n=3–11). *P<0.05; **P<0.01 versus p53+/+ AS; ##P<0.01 versus p53+/− AS.