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. 2021 Aug 9;6(15):e148109. doi: 10.1172/jci.insight.148109

Figure 1. Induction of Twist1 in podocytes from patients with podocytopathies and mice with NTS- or ADR-induced glomerular disease.

Figure 1

(A) Representative IHC staining of Twist1 in renal biopsies from patients with FSGS, IgA nephropathy, or DN or normal control subjects. Scale bar: 50 μm. (B and C) Twist1 mRNA (B) and protein abundance (C) in glomeruli isolated from mice on day 9 after NTS-induced glomerulonephritis (n = 3–7, Wilcoxon’s test). (D) Semiquantitative determination of Twist1 protein from blots in C (n = 3, t test). (E) Representative Twist1- and nephrin-costained kidney sections from vehicle- and NTS-treated animals. (F and G) Twist1 mRNA (F) and protein abundance (G) in glomeruli isolated from mice on day 4 after ADR-induced glomerular injury (n = 3–7, Wilcoxon’s test). (H) Semiquantitative determination of Twist1 protein from blots in G (n = 3, t test). (I) Representative Twist1- and nephrin-costained kidney sections from vehicle- and ADR-treated mice. Scale bar: 40 μm. Data represent mean ± SEM. All t tests were 2 tailed. *P < 0.05. veh, vehicle; NTS, nephrotoxic serum; ADR, adriamycin; FSGS, focal segmental glomerulosclerosis; DN, diabetic nephropathy.