MicroRNA‐126 regulates EPCs function: Implications for a role of miR‐126 in preeclampsia

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Abstract
Preeclampsia is a specific vascular complication in pregnancy, which has a pathophysiology of altered endothelial homeostasis. There is extensive evidence that endothelial progenitor cells (EPCs) dysfunction underlies the endothelial cells loss that occurs during preeclampsia. MicroRNA‐126 (miR‐126), an angiogenesis‐related miRNA, has been shown to have potential angiogenic effects both in cultured endothelial cells in vitro and ischemia‐induced angiogenesis in vivo. However, whether miR‐126 has therapeutic potential in placental vasculogenesis of preeclampsia remains unclear. In this report, we analyzed the EPCs number and expression of miR‐126 in patients with preeclampsia, then investigated the effects of miR‐126 on EPCs function and rat placenta by employing up‐regulation and down‐regulation strategies. We confirmed that miR‐126 enhanced EPCs proliferation, differentiation and migration. However, a strong reduction in EPCs function was observed in vitro after miR‐126 inhibitor transfection. MiR‐126 exerts pro‐angiogenic functions by suppressing the synthetize of antiangiogenic factors PIK3R2. Similar to miR‐126 overexpression, PIK3R2 downregulation promoted EPCs function. In pregnant rats, we also found that miR‐126 increased vascular sprouting, placenta and fetus weights. These findings suggest that miR‐126 is essential for angiogenic properties of EPCs in vitro and placental vasculogenesis in vivo, providing basis for an alternative therapeutic approach in patients with preeclampsia. J. Cell. Biochem. 114: 2148–2159, 2013.

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