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. 2019 May 2;4(9):e124747. doi: 10.1172/jci.insight.124747

Figure 4. Decrease of SIRPα in podocytes of mice and humans under nephropathy.

Figure 4

(A) SIRPα level in glomerulus of mice with PAN, ADR, and STZ treatment over time. Immunoblots are representative of 3 independently performed experiments. Histograms show quantification of SIRPα level. (B) Immunofluorescence staining of SIRPα and nephrin in glomerulus of mice treated with PAN, ADR, and STZ for 2, 4, and 6 weeks (W) respectively. Quantification of SIRPα and nephrin levels in glomerulus was performed by counting approximately 10 glomeruli from 3 independent determinations. Data in A and B represent mean ± SEM from 3 independent experiments, and P value was analyzed by ANOVA with Tukey-Kramer test and 2-tailed Student’s t test, respectively. (C) Colocalization and expression level of SIRPα and nephrin in podocytes of healthy control and FSGS patients. (D) Glomerular immunohistochemistry staining of SIRPα in FSGS patients with low proteinuria (n = 9) and with high proteinuria (n = 8). Histogram represents quantification of glomerular SIRPα staining in the 2 groups of patients. Data represent mean ± SEM, and P value was analyzed by 2-tailed Student’s t test. (E, F, and G) Correlation analysis between SIRPα and albumin level, albumin/creatinine ratio (A/C), and podocyte number; r and P values were analyzed by Pearson’s correlation analysis; red and black plots represent FSGS patients with low and high proteinuria, respectively. In Scale bars in B, C, and D: 25 μm.**P < 0.01.