基因敲除
滋养层
细胞生长
体内
子痫前期
男科
医学
胎盘
发病机制
癌症研究
体外
小RNA
细胞培养
内科学
生物
基因
怀孕
胎儿
遗传学
作者
Xudong Zhao,Fengyun Su,Fanhua Kong,Qing Guo,Xiaogang Wang,Hong Cui,Qinwen Li,Wangmeng Zhang,Lei Li,Aihua Li
摘要
Abstract Background Decreased proliferation and invasion of trophoblast were proven to be involved in the pathogenesis of preeclampsia (PE). However, the regulatory network has not been clarified yet. This study aimed to explore the role of miR‐101‐3p in the progression of PE. Methods miR‐101‐3p expression in placentas of pregnant women with or without PE was analyzed by real‐time quantitative PCR (RT‐qPCR). Trophoblastic HTR‐8/SVneo and HPT‐8 cell lines were cultured and underwent hypoxia/reoxygenation (H/R) treatment to mimic PE in vitro. Cell proliferation and invasion were analyzed in gain‐of and loss‐of‐function assays. Finally, we undertook in vivo studies to explore effects of miR‐101‐3p in the PE model. Results Compared to placentas from patients without PE, miR‐101‐3p expressed significantly higher in placentas from PE patients, and its level was positively correlated with the severity of patients. In vitro studies found that overexpression of miR‐101‐3p significantly suppressed cell proliferation and invasion, while knockdown of miR‐101‐3p reversed the impacts of H/R treatment. Further research showed that the expression of WD repeat domain 5 (WDR5) was significantly lower in placentas from patients with PE, and its level was negatively associated with the severity of patients. In vitro and in vivo studies confirmed that miR‐101‐3p promoted PE progression through the regulation of WD WDR5 expression. Conclusion Increased expression of miR‐101‐3p in placenta contributes to the development of PE by suppressing WDR5‐mediated proliferation and invasion of trophoblast.
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