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首页> 外文期刊>The journal of obstetrics and gynaecology research >MiR‐342‐3p inhibition promotes cell proliferation and invasion by directly targeting ID4 in pre‐eclampsia
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MiR‐342‐3p inhibition promotes cell proliferation and invasion by directly targeting ID4 in pre‐eclampsia

机译:MiR-342-3P抑制促进细胞增殖和直接靶向ID4在预先普利坦斯预先靶向

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Abstract Aim This study aimed to explore the miR‐342‐3p expression in pre‐eclampsia (PE) placentas and confirm whether miR‐342‐3p exerts effects on proliferation and migration of HTR‐8/SVneo trophoblastic cells. Methods The PE placentas ( n = 8) were taken from gravidas complicated by PE and delivered after 34?weeks. The chorionic plates and the basal plates were separately taken from the placenta disc near the position of umbilical cord insertion. RT‐qPCR was used to measure the expression of miR‐342‐3p in the chorionic plates and the basal plates. Cell invasion assay and MMT assay were used to assess the effects of miR‐342‐3p on proliferation and migration of HTR‐8/SVneo trophoblastic cells. Luciferase reporter assay and Western blotting were used to analyze the target of miR‐342‐3p and investigate the detailed mechanisms. Results The expression of miR‐342‐3p was upregulated in both basal plates and chorionic plates in patients with PE compared with healthy pregnant individuals. MiR‐342‐3p inhibitor suppressed the cell viability and invasion, and induced apoptosis in trophoblast cells. Furthermore, inhibitor of DNA binding (ID)‐4 (ID4) was a direct target of miR‐342‐3p, and knockdown of ID4 abrogated the regulation effect of miR‐342‐3p on cell viability, apoptosis and invasion. Conclusion Inhibition of miR‐342‐3p expression may suppress the occurrence of PE by targeting ID4 in vitro .
机译:摘要目的本研究旨在探讨miR-342-3p在子痫前期(PE)胎盘中的表达,并确认miR-342-3p是否对HTR-8/SVneo滋养层细胞的增殖和迁移产生影响。方法8例PE胎盘均取自合并PE的孕妇,34天后分娩?周。绒毛膜板和基板分别取自胎盘盘靠近脐带插入位置处。RT-qPCR用于测量绒毛膜板和基板中miR-342-3p的表达。细胞侵袭试验和MMT试验用于评估miR-342-3p对HTR-8/SVneo滋养层细胞增殖和迁移的影响。荧光素酶报告分析法和Western印迹法用于分析miR-342-3p的靶点并研究其详细机制。结果与健康孕妇相比,PE患者的基板和绒毛膜板中miR-342-3p的表达均上调。MiR-342-3p抑制剂抑制滋养层细胞的存活和侵袭,并诱导细胞凋亡。此外,DNA结合抑制剂(ID)-4(ID4)是miR-342-3p的直接靶点,而ID4的敲除消除了miR-342-3p对细胞活力、凋亡和侵袭的调节作用。结论抑制miR-342-3p表达可能通过体外靶向ID4抑制PE的发生。

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