miR-30b facilitates preeclampsia through targeting MXRA5 to inhibit the viability, invasion and apoptosis of placental trophoblast cells.

Preeclampsia (PE) may induce gestational failure threatening a significant number of pregnant women. Dysfunctional placental trophoblast cells have an important impact on PE progression. microRNAs (miRNAs) have been reported to participate in PE progression, whereas the mechanism that underlies miR-30b involved in PE progression and function of placental trophoblast cells remains poorly understood. Cell viability was investigated by cell counting kit-8 (CCK-8) assay. Cell apoptosis was detected by flow cytometry using Annexin V-FITC/propidium iodide (PI) staining. Cell invasion was analyzed by trans-well assay. The expression of miR-30b was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The abundance of matrix-remodeling associated 5 (MXRA5) protein was detected by western blots (WB). The interaction between miR-30b and MXRA5 was investigated by bioinformatics analysis and luciferase activity assay. The effect of miR-30b and MXRA5 on mitogen-activated protein kinases (MAPK) pathway and invasion was evaluated by WB. Then we found miR-30b was highly expressed in PE and its overexpression inhibited cell viability and invasion while enhanced apoptosis in JEG-3 and HTR8/SVneo cells. Moreover, MXRA5 was targeted by miR-30b and MXRA5 restoration attenuated the effect of miR-30b on cell processes in HTR8/SVneo cells. Besides, both of miR-30b and MXRA5 were associated with MAPK pathway in HTR8/SVneo cells. Our data suggested miR-30b might contribute to PE through inhibiting cell viability, invasion while inducing apoptosis of placental trophoblast cells via MAPK pathway by targeting MXRA5. These indicated that miR-30b might be a novel biomarker for PE treatment.