Preeclampsia (PE) is a major risk factor for maternal and fetal mortality. Studies showed that microRNAs (miRNAs) play important roles in PE, and are closely related to extra-villous trophoblastic proliferation and invasion. The current study determined miR-125b expression in PE patients, and explored the role of miR-125b in the occurrence and development of PE and its possible mechanism, aiming to provide a novel basis for the diagnosis and treatment of PE. The level of miR-125b in serum derived from pregnant women was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, invasion and migration of HTR-8/SVneo were determined by Cell Counting Kit-8 (CCK-8), Transwell and scratch assay, respectively. The target gene of miR-125b was predicted by Targetscan, and verified by luciferase reporter assay. The expressions of related proteins were determined by Western Blotting. The miR-125b level in the serum of PE patients was up-regulated as compared with normal pregnant women, and high level of miR-125b reduced cell proliferation, inhibited invasion and migration of HTR-8/SVneo as well as the expressions of STAT3, p-STAT3 and SOCS3, while low level of miR-125b produced the opposite results. STAT3 was predicted as the target gene of miR-125b, and the high level of miR-125b inhibited STAT3 signaling pathway. High expression of miR-125b may be involved in the occurrence of PE through inhibiting STAT3 pathway to inhibit the migration and invasion of extra-villous trophoblastic cells.

中文翻译：

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MiR-125b通过STAT3信号通路调控绒毛外滋养细胞的迁移和侵袭参与子痫前期的发生

先兆子痫（PE）是孕产妇和胎儿死亡的主要危险因素。研究表明，microRNAs（miRNAs）在PE中发挥重要作用，与绒毛外滋养细胞的增殖和侵袭密切相关。本研究测定了PE患者miR-125b的表达情况，探讨了miR-125b在PE发生发展中的作用及其可能机制，旨在为PE的诊治提供新的依据。通过定量实时聚合酶链反应 (qRT-PCR) 测量孕妇血清中 miR-125b 的水平。HTR-8/SVneo 的细胞增殖、侵袭和迁移分别通过 Cell Counting Kit-8 (CCK-8)、Transwell 和 Scratch 试验测定。miR-125b的靶基因由Targetscan预测，并通过荧光素酶报告基因检测进行验证。Western Blotting检测相关蛋白的表达。PE患者血清中miR-125b水平较正常孕妇上调,高水平miR-125b降低细胞增殖、抑制HTR-8/SVneo侵袭迁移及STAT3表达、p-STAT3 和 SOCS3，而低水平的 miR-125b 产生相反的结果。STAT3被预测为miR-125b的靶基因，高水平的miR-125b抑制了STAT3信号通路。miR-125b的高表达可能通过抑制STAT3通路抑制绒毛外滋养细胞的迁移和侵袭参与PE的发生。和高水平的 miR-125b 降低细胞增殖，抑制 HTR-8/SVneo 的侵袭和迁移以及 STAT3、p-STAT3 和 SOCS3 的表达，而低水平的 miR-125b 产生相反的结果。STAT3被预测为miR-125b的靶基因，高水平的miR-125b抑制了STAT3信号通路。miR-125b的高表达可能通过抑制STAT3通路抑制绒毛外滋养细胞的迁移和侵袭参与PE的发生。和高水平的 miR-125b 降低细胞增殖，抑制 HTR-8/SVneo 的侵袭和迁移以及 STAT3、p-STAT3 和 SOCS3 的表达，而低水平的 miR-125b 产生相反的结果。STAT3被预测为miR-125b的靶基因，高水平的miR-125b抑制了STAT3信号通路。miR-125b的高表达可能通过抑制STAT3通路抑制绒毛外滋养细胞的迁移和侵袭参与PE的发生。