MiR-134 inhibits infiltration of trophoblast cells in placenta of patients with preeclampsia by decreasing ITGB1 expression

A.-X. Zou, B. Chen, Q.-X. LI, Y.-C. Liang

Department of Obstetrics, The Children & Women’s Healthcare of Laiwu City, Laiwu, China. ziluz72589075@163.com

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• Obstetrics

OBJECTIVE: Preeclampsia (PE) is an idiopathic disorder of pregnancy. The specific regulatory mechanisms of microRNAs (miRs) in the placenta of PE patients have not yet been completely revealed. This study mainly explored the mechanism of miR-134 in preeclampsia.

PATIENTS AND METHODS: Real-time PCR and Western blot were used to detect the expression of miR-134 and ITGB1 in the placenta of patients with preeclampsia and normal pregnant women. Dual luciferase reporter assay was performed to detect luciferase activity in miR-134 and NC groups, respectively. Cell proliferation ability after transfection was evaluated by MTS colorimetric assay, and the effect of miR-134 on the infiltration of trophoblast cells was explored by cell invasion experiment. In addition, co-transfection of miR-134 and ITGB1 expression plasmids was carried out, and then changes in the cell invasiveness were also detected by cell invasion experiment.

RESULTS: Compared with placenta of normal pregnant women, miR-134 was significantly up-regulated in the placenta of patients with preeclampsia and negatively correlated with the expression of ITGB1. MiR-134 suppressed the infiltration of trophoblast cells by targeting ITGB1. When ITGB1 was overexpressed, the suppression of invasiveness of trophoblast cells by miR-134 was almost abolished. Meanwhile, we found that miR-134 inhibitor could promote the invasiveness of trophoblast cells. In addition, tumor necrosis factor-α (TNF-α) was found to enhance miR-134 expression as well as inhibit ITGB1 expression.

CONCLUSIONS: MiR-134 inhibited the infiltration of trophoblast cells in preeclampsia by down-regulating ITGB1 expression.

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