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

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FIG. 1.
FIG. 1.

HG induces podocyte apoptosis through activation of mTOR. Mouse podocytes were serum deprived overnight and pretreated with rapamycin (Rapa) (10 nmol/L) for 1 h before incubation with HG for 48 h. Mannitol was used as osmotic control. Rapamycin treatment inhibits HG-induced apoptosis as measured by annexin V binding (A), caspase 3 activity (B), cellular DNA fragmentation (C), and Hoechst staining (D). E: Quantification of Hoechst-positive cells (% of apoptosis) from four different experiments. Rapamycin treatment also inhibited the mTOR/S6K pathway. F: Representative Western blot of p-p70S6KThr389, p70S6K, p-mTORSer2448, mTOR, and β-actin levels. G: Histograms showing quantitation of p-p70S6KThr389/p70S6K results from four different experiments. H: Histograms showing quantitation of p-mTORSer2448/mTOR results from four different experiments. I: Representative Western blot of p-AMPKThr172 and AMPK levels. J: Histograms showing quantitation of p-AMPKThr172/AMPK results from four different experiments. 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