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. 2019 Sep 19;4(18):e99271. doi: 10.1172/jci.insight.99271

Figure 7. Pharmacological inhibition of mTOR signaling impairs podocyte hypertrophy and leads to FSGS.

Figure 7

(A) Schematic representation of experimental design. (B) Representative confocal images after indirect immunofluorescence showing pharmacological inhibition of ribosomal protein S6 phosphorylation (p-rp-S6; green) in podocytes (Synaptopodin; SNP in red). (C) Urinary albumin to creatinine ratio (UACR). (D) Periodic acid–Schiff (PAS) histological stainings showing glomerulosclerosis in mTOR-treated mice during induction of podocyte loss. (E) Percentage of pathological glomeruli. (F) Representative confocal images after indirect immunofluorescence showing de novo PEC activation (CD44 upregulation; green) in mice treated with mTOR inhibitors during induction of podocyte loss via diphtheria toxin (DT) administration. (G) Podocyte number. (H) Total podocyte volume per unit of podocyte density (TPV:PD ratio). ****P < 0.0001; ***P < 0.001; **P < 0.01. In C and E, circles and bars represent means and error bars ± SEM. In violin plots, red lines represent medians and blue lines represent IQRs; every gray dot represents 1 glomerulus. Kruskal-Wallis with Dunn’s multiple comparisons tests were used. Scale bars: (B) 30 μm, (D) 60 μm, and (F) 50 μm.

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