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MicroRNA-16 is involved in the pathogenesis of preeclampsia via regulation of Notch2

机译:MicroRNA-16的发病机制通过监管Notch2子痫前期

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In recent years, the role of microRNAs (miRNAs) in pre-eclampsia (PE) has been demonstrated, while the relevant mechanisms of miR-16 in PE await to be unearthed. Thus, the aim of this study is to explore whether miR-16 exerts its function in PE, and we assumed that miR-16 may be implicated in the occurrence of PE by adjusting the biological functions of trophoblast cells via modulating Notch2. Placental tissues of pregnant women with normal pregnancy and PE were collected to detect the expression of miR-16, Notch2, and Notch3. The effects of miR-16 and Notch2 on the biological functions of BeWo and JEG-3 cells were further determined. Expression of miR-16 and Notch2 in trophoblast cells was detected by reverse transcription quantitative polymerase chain reaction and western blot assay. Downregulated Notch2 and upregulated miR-16 and Notch3 were found in placental tissues of PE. There was a negative correlation between Notch2 and miR-16 expression (r = -0.769), and a positive correlation between Notch3 and miR-16 expression (r = 0.676; p < .05). Overexpression of miR-16 inhibited proliferation, migration, and invasion, and facilitated the apoptosis of BeWo and JEG-3 cells, but overexpression of Notch2 reversed this trend. Overexpression of miR-16 inhibited Notch2 expression in BeWo and JEG-3 cells, and Notch2 was the target gene of miR-16. Our study highlights that overexpression of miR-16 is involved in PE by regulating the biological functions of trophoblast cells via inhibition of Notch2. This paper provides a new idea for further study of the pathogenesis of PE.
机译:近年来,小分子核糖核酸(microrna)的作用先兆子痫(PE)已经证明,在PE等待miR-16的相关机制被发现了。探索miR-16是否发挥体育的功能,我们假定miR-16可能涉及PE的发生通过调整生物通过调节滋养层细胞的功能Notch2。正常妊娠和PE收集检测的表达miR-16、Notch2 Notch3。miR-16和Notch2生物的影响BeWo JEG-3细胞进一步的函数确定。滋养层细胞被逆转转录定量聚合酶链反应和免疫印迹分析。Notch2和调节miR-16 Notch3PE的胎盘组织中发现的。Notch2和miR-16之间负相关表达式(r = -0.769),和积极的Notch3和miR-16表达之间的相关性(r = 0.676;抑制细胞增殖、迁移和入侵,和促进细胞凋亡BeWo JEG-3细胞,但是过度的Notch2逆转的趋势。在BeWo和JEG-3细胞表达,Notch2miR-16的目标基因。突出了miR-16的过度参与体育通过调节生物通过抑制滋养层细胞的功能Notch2。对PE的发病机制的进一步研究。

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