Li Qinghua, Pan Zhifang, Wang Xuejian, Gao Zhiqin, Ren Chune, Yang Weiwei
Public Health College, Weifang Medical University, Weifang 261053, China.
School of Biological Sciences, Weifang Medical University, Weifang 261053, China.
Biochem Biophys Res Commun. 2014 Oct 10;453(1):57-63. doi: 10.1016/j.bbrc.2014.09.059. Epub 2014 Sep 22.
Preeclampsia (PE) is the leading cause of maternal and perinatal mortality and morbidity. Understanding the molecular mechanisms underlying placentation facilitates the development of better intervention of this disease. MicroRNAs are strongly implicated in the pathogenesis of this syndrome. In current study, we found that miR-125b-1-3p was elevated in placentas derived from preeclampsia patients. Transfection of miR-125b-1-3p mimics significantly inhibited the invasiveness of human trophoblast cells, whereas miR-125b-1-3p inhibitor enhanced trophoblast cell invasion. Luciferase assays identified that S1PR1 was a novel direct target of miR-125b-1-3p in the placenta. Overexpression of S1PR1 could reverse the inhibitory effect of miR-125b-1-3p on the invasion of trophoblast cells. These findings suggested that abnormal expression of miR-125b-1-3p might contribute to the pathogenesis of preeclampsia.
子痫前期（PE）是孕产妇和围产儿发病及死亡的主要原因。了解胎盘形成的分子机制有助于开发针对该疾病的更好干预措施。微小RNA与该综合征的发病机制密切相关。在本研究中，我们发现子痫前期患者胎盘组织中miR-125b-1-3p表达上调。转染miR-125b-1-3p模拟物可显著抑制人滋养层细胞的侵袭能力，而miR-125b-1-3p抑制剂则增强滋养层细胞的侵袭能力。荧光素酶报告基因实验确定S1PR1是胎盘组织中miR-125b-1-3p的一个新的直接靶点。过表达S1PR1可逆转miR-125b-1-3p对滋养层细胞侵袭的抑制作用。这些研究结果提示，miR-125b-1-3p的异常表达可能参与了子痫前期的发病过程。
