Introduction: Pre-eclampsia is characterized by insufficient spiral artery remodeling, and trophoblast dysfunction plays an important role in this process. Noncoding RNAs (microRNAs (miRNAs) and long noncoding RNAs (LncRNAs) are included) can regulate trophoblasts. MicroRNA-210 (miR-210) can decrease trophoblast cell migration and invasion and may act as a biomarker for preeclampsia. LncRNA maternally expressed gene 3 (MEG3) plays a positive role in pre-eclampsia, and MEG3 can be a downstream target of miR-210 in human umbilical vein endothelial cells (HUVEC). However, the effect of miR-210 on MEG3 and the mechanism of action of the miR-210/MEG3 axis in trophoblasts remain unclear.
Method: The localization of miR-210 and MEG3 in the human placenta in early pregnancy was determined by in situ hybridization. Then, HTR8/SVneo cells were used to investigated the effect of miR-210 on MEG3 expression and biological activity of trophoblasts in the migration and invasion assays. Gain- and loss-of-function experiments were performed to determine the mechanism of action of miR-210 and MEG3 in Epithelial-mesenchymal transition (EMT) of HTR8/SVneo cells.
Results: The qRT-PCR and western blotting results demonstrated that the upregulation of miR-210 decreases MEG3, N-cadherin and Vimentin expression and increases E-cadherin expression to inhibit EMT in HTR-8/SVneo cells. Inhibition of the expression of miR-210 results in the opposite effects. Gain- and loss-of-function assay indicated that miR-210 can impair the EMT, migration, and invasion of HTR8/SVneo cells by regulating the expression of MEG3.
Disscussion: MiR-210 may be a negative regulator of trophoblast EMT that acts by suppressing MEG3 expression.
Keywords: Epithelial-mesenchymal transition (EMT); LncRNA maternally expressed gene 3 (MEG3); Pre-eclampsia; Trophoblast; microRNA-210 (miR-210).
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