[Retracted] Knockdown of miR-372-3p Inhibits the Development of Diabetic Cardiomyopathy by Accelerating Angiogenesis via Activating the PI3K/AKT/mTOR/HIF-1α Signaling Pathway and Suppressing Oxidative Stress

Figure 5

Involvement of the PI3K signaling pathway in miR-372-3p KD-induced angiogenesis in HG-stimulated C166 cells. (a) Protein expressions of p-PI3K, PI3K, p-AKT, AKT, mTOR, p-mTOR, P70S6K, p-P70S6K, and HIF-1α in the control, model, and miR-372-3p KD groups treated with or without LY294002. β-Actin was considered as a loading control, and the statistical analysis was performed to present the p-PI3K, PI3K, p-AKT, AKT, mTOR, p-mTOR, P70S6K, p-P70S6K, and HIF-1α in the control, model, and miR-372-3p KD groups with or without LY294002. (b) Protein expressions of NOX2 and NOX4 in the control, model, and miR-372-3p KD groups treated with or without LY294002. β-Actin was considered as a loading control, and the statistical analysis was performed to present the NOX2 and NOX4 in the control, model, and miR-372-3p KD groups with or without LY294002. (c) The number of tubes formed in each group. Data were presented as , Bar: 200 μM, /group, and : model group vs. miR-372-3p KD group.

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