Lentivirus-mediated miR-23a overexpression induces trophoblast cell apoptosis through inhibiting X-linked inhibitor of apoptosis

Publication date: October 2017
Source:Biomedicine & Pharmacotherapy, Volume 94
Author(s): Lichun Li, Aiqin Hou, Xia Gao, Juan Zhang, Liping Zhang, Juan Wang, Hua Li, Yanbin Song
Preeclampsia (PE) is a pregnancy-specific disorder representing a major cause of maternal and perinatal morbidity and mortality. MicroRNAs (miRNAs) have emerged as critical regulators in PE. However, the precise role of miRNAs in PE remains poorly understood. In this study, we aimed to investigate the potential role of miR-23a and the underlying mechanism in regulating trophoblast cell apoptosis. We found a significant increase of miR-23a expression in placental tissues from PE patients. Lentivirus-mediated miR-23a overexpression significantly induced apoptosis in trophoblast cells in vitro. X-linked inhibitor of apoptosis (XIAP) was identified as a target gene of miR-23a by bioinformatics analysis and dual-luciferase reporter assay. Overexpression of miR-23a significantly inhibited XIAP expression. Knockdown of XIAP also induced trophoblast cell apoptosis. Moreover, restoration of XIAP expression significantly abolished the miR-23 overexpression-induced trophoblast cell apoptosis. Taken together, our study demonstrates that miR-23a induces trophoblast cell apoptosis by inhibiting XIAP, which may contribute to PE. Our findings provide novel insights into understanding the pathogenesis of PE and suggest a potential therapeutic target in PE.



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