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

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FIG. 2.FIG. 2.
FIG. 2.

HG regulates mTOR through AMPK to induce podocyte apoptosis. Podocytes were exposed to 25 mmol/L glucose (HG) with or without AICAR (1 mmol/L) for 48 h. In parallel experiments, podocytes were exposed to HG with or without rapamycin (Rapa) (10 nmol/L) for 48 h. Mannitol was used as osmotic control. A: Representative Western blot of p-p70S6KThr389, p70S6K, and β-actin levels. B: Histograms showing quantitation of p-p70S6KThr389/p70S6K results from four different experiments. C: Representative Western blot of p-mTORSer2448, mTOR, and β-actin levels. D: Histograms showing quantitation of p-mTORSer2448/mTOR results from four different experiments. E: Representative Western blot of p-AMPKThr172, AMPK, and β-actin levels. F: Histograms showing quantitation of p-AMPKThr172/AMPK results from four different experiments. G: Histograms representing AMPK activity measured in podocytes treated with HG in the presence or absence of AICAR. H: Representative Western blot of p-TSC2Thr1462, p-TSC2Ser1387, TSC2, and β-actin levels. Histograms showing quantitation of p-TSC2Thr1462/TSC2 (I), p-TSC2Ser1387/TSC2 (J), and TSC2/β-actin (K) (n = 4). L: Representative Western blot of p-TSC2Ser1387and β-actin levels. M: Histograms showing quantitation of p-TSC2Ser1387/β-actin (n = 4). All values are the mean ± SE from four independent experiments. *P < 0.05 vs. control; #P < 0.05 vs. HG.

This Article

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