Mammalian Target of Rapamycin Regulates Nox4-Mediated Podocyte Depletion in Diabetic Renal Injury

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FIG. 6.
FIG. 6.

mTOR/S6 kinase activation upregulates Nox4 and enhances NADPH oxidase activity in type 1 diabetes. OVE26 mice (17 weeks old) were treated with rapamycin (Rapa) (0.5 mg/kg body weight) for 5 weeks (3 times/week). Mice in the control group received saline vehicle. Glomeruli were isolated from the kidneys of FVB control mice, OVE26 mice, and OVE26 mice treated with rapamycin (n = 5 mice/group). A: Relative mRNA levels of Nox4 in control FVB, OVE26, and OVE26 mice treated with rapamycin. B: Representative Western blot of Nox4 and β-actin levels. C: Histograms showing Nox4/β-actin quantitation of results from five mice. D: Nox4 expression and localization were detected by immunoperoxidase staining of kidney sections from control FVB (a), OVE26 (b), and OVE26 (c) mice treated with rapamycin. E: NADPH-dependent superoxide generation. All values are the means ± SE from five animals for each group. *P < 0.05, OVE26 mice vs. FVB mice; #P < 0.05, rapamycin-treated OVE26 mice vs. vehicle-treated OVE26 mice.

This Article

  1. Diabetes vol. 62 no. 8 2935-2947