Abstract
Aim: To explore the underlying mechanisms of metformin on the angiogenic capacity of endothelial progenitor cells (EPCs). Results: EPC growth and miR-221 expression decreased concentration-dependence with metformin, and a negative correlation was observed between miR-221 expression and metformin concentration (p <0.001). miR-221 overexpression using a mimic decreased the metformin-mediated angiogenic effects in EPCs (p <0.01). Metformin increased p27 and LC3II expression and AMP-activated protein kinase (AMPK) phosphorylation, and decreased p62 expression, while miR-221 overexpression reversed the effects of metformin. Additionally, AMPK inhibition by compound C reversed the increase in p27 and LC3II levels and AMPK phosphorylation or miR-221 siRNA treatment. Conclusion: Metformin inhibits the angiogenic capacity of EPCs. The underlying mechanism involves AMPK-mediated autophagy pathway activity and increases miR-221-mediated p27 expression.
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