Abstract:

Objective To explore the mechanism of microRNA （miRNA）-365a-3p affecting the function of vascular endothelial cells involved in the pathogenesis of preeclampsia （PE）. Methods Primary human umbilical vein endothelial cells （HUVECs） were set as a NC group （transfected miR-365a-3p NC）， a mimics group （transfected miR-365a-3p mimics） and a inhibitor group （transfected miR-365a-3p inhibitor）. Logarithmic HUVECs cells were set as the blank group. The cell proliferation， migration and angiogenesis in each group were detected. Dual luciferin assay verified the targeting relationship between miR-365a-3p and downstream gene. The protein expressions of TGF-β₁， Smad4 and Smad7 in each group were detected. Results Compared with the blank group and the NC group， the absorbance value and mobility of 24， 48 and 72 h were decreased （P < 0.05）， the number of tubular structures per field were decreased in the mimics group （P < 0.05）， the absorbance value and mobility of 24， 48 and 72 h were increased （P < 0.05）， and the number of tubular structures per field were increased in the inhibitor group （P < 0.05）. Dual luciferin assay showed that Smad7 was a target gene of miR-365a-3p. Compared with the blank group and the NC group， the protein expressions of TGF-β₁ and Smad4 in the mimics group were increased （P < 0.05）， while the protein expression of Smad7 was decreased （P < 0.05）. The protein expression levels of TGF-β₁ and Smad4 in the inhibitor group were decreased （P < 0.05）， while the protein expression levels of Smad7 were increased （P < 0.05）. Conclusion miR-365a-3p may affect the function of vascular endothelial cells by regulating the downstream TGF-β signaling pathway， and thus participate in the pathogenesis of PE.

Key words: preeclampsia, microRNA-365a-3p, vascular endothelial cell function, transforming growth factor beta