MiR-200c regulates apoptosis of placental trophoblasts in preeclampsia rats through Wnt/β-catenin signaling pathway.

Abstract

To investigate the influence of micro ribonucleic acid 200c (miR-200c) on the apoptosis of placental trophoblasts in a rat model of preeclampsia (PE). PE model in rats was established for extracting placental trophoblasts. Overexpression or knockdown of miR-200c was achieved by transfection of miR-200c mimics or inhibitor. Flow cytometry was carried out to detect the apoptotic rate of placental trophoblasts. Dual-luciferase reporter gene assay was performed to detect the interaction of miR-200c with WNT1. Western blotting was applied to determine the changes of protein levels in placental trophoblasts. The expression level of miR-200c in placental trophoblasts of PE group was significantly higher than that in control group. The apoptosis rate was (22.45 ± 2.62)%, (6.58 ± 1.28)%, and (9.57 ± 1.35)% in miR-200c mimic group, miR-200c inhibitor group, and control group, respectively, showing statistically significant differences. MiR-200c overexpression downregulated the expression level of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), but upregulated expression levels of apoptotic proteins Bcl-2-associated X protein (Bax) and active Caspase-3. MiR-200c suppressed WNT1 expression through the interaction with the 3'-untranslated region (3'-UTR) of WNT1. The expressions of WNT1 and β-catenin were up-regulated after miR-200c overexpression, which was reversed by the Wnt/β-catenin pathway activator. MiR-200c is involved in the development and progression of PE through the Wnt/β-catenin signaling pathway.