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

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

FIG. 5.
FIG. 5.

Decrease in the phosphorylation and activation of AMPK inactivates TSC2 and activates the mTOR/S6K pathway and leads to podocyte injury in type 1 diabetes. OVE26 mice (17 weeks old) were treated with AICAR (750 mg/kg/day, dissolved in saline, i.p.) for 5 weeks. Mice in the control group received saline vehicle. Glomeruli were isolated from the kidneys of three groups of mice (n = 5): FVB control mice, OVE26 mice, and OVE26 mice treated with AICAR. A: Representative Western blot of p-AMPKαThr172 and total AMPKα from isolated glomeruli of control FVB mice, OVE26 mice, and OVE26 mice treated with AICAR. B: Histograms showing quantitation of results from 5 mice. C: Histograms showing AMPK activity. D: Representative Western blot of p-p70S6KThr389, p70S6K, p-mTORSer2448, and mTOR. Histograms showing quantitation of results for p-p70S6K/p70S6K (E) and p-mTOR/mTOR (F) from five mice. G: Representative Western blot of p-TSC2Ser1387, TSC2, and β-actin levels. Histograms showing quantitation of results for p-TSC2Ser1387/β-actin (H) and TSC2/β-actin (I) from five mice. All values are the means ± SE from five animals for each group. *P < 0.05 OVE26 mice vs. FVB mice; #P < 0.05 AICAR-treated OVE26 mice vs. vehicle-treated OVE26 mice.

This Article

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