MiR-200b-3p is upregulated in the placental tissues from patients with preeclampsia and promotes the development of preeclampsia via targeting profilin 2

MiR-200b-3p 在先兆子痫患者的胎盘组织中上调,并通过靶向 profilin 2 促进先兆子痫的发展

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作者:Huijun Liu, Xietong Wang

Abstract

Preeclampsia is a serious pregnancy disorder affecting both maternal and fetal health. However, the pathogenesis of preeclampsia has not been fully understood. This study aimed to investigate the key microRNAs (miRNAs) in the development of preeclampsia. A high-throughput miRNA sequencing analysis for the placental tissues from patients with preeclampsia and healthy controls was conducted, followed by investigation of differentially expressed miRNAs (DEMs) and functional enrichment analysis. Moreover, the expression of a key DEM, named miR-200b-3p, in the preeclampsia patients was validated, and the effects of miR-200b-3p overexpression on the proliferation, migration, and apoptosis of HTR8 trophoblast cells were investigated in vitro. Furthermore, the target gene of miR-200b-3p was investigated based on gene expression profile GSE177049 and miRWalk 2.0 database. The target relationship between miR-200b-3p and profilin 2 (PFN2) was investigated in vitro. A total of 12 DEMs including miR-200b-3p were identified between preeclampsia placental tissues and control placental tissues, which were significantly enriched in several pathways, such as cell adhesion molecules (CAMs) and tight junction. Moreover, increased expression of miR-200b-3p was revealed in the placental tissues of preeclampsia patients, and overexpression of miR-200b-3p suppressed cell proliferation and migration but promoted apoptosis of trophoblast cells. Furthermore, PFN2 was confirmed as a target of miR-200b-3p, and overexpression of PFN2 reversed the inhibitory effects of miR-200b-3p overexpression on trophoblast cell migration. Our findings reveal that miR-200b-3p is upregulated in the placental tissues of patients with preeclampsia and promotes preeclampsia development via PFN2. miR-200b-3p may serve as a promising therapeutic target against preeclampsia.

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