Department of Obstetrics, Affiliated Hospital, Yan'an University, Yan'an, Shaanxi 716000, China.
Department of Obstetrics, Affiliated Hospital, Yan'an University, Yan'an, Shaanxi 716000, China.
Biomed Pharmacother. 2017 Oct;94:412-417. doi: 10.1016/j.biopha.2017.07.082. Epub 2017 Aug 1.
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.
子痫前期 (PE) 是一种妊娠特有的疾病，是孕产妇和围生儿发病率和死亡率的主要原因。微小 RNA（miRNA）已成为调节子痫前期的关键调控因子。然而，miRNA 在子痫前期中的确切作用仍知之甚少。在这项研究中，我们旨在研究 miR-23a 在调节滋养细胞凋亡中的潜在作用及其潜在机制。我们发现子痫前期患者胎盘组织中 miR-23a 的表达显著增加。慢病毒介导的 miR-23a 过表达在体外显著诱导滋养细胞凋亡。通过生物信息学分析和双荧光素酶报告基因实验鉴定出 X 连锁凋亡抑制剂 (XIAP) 是 miR-23a 的靶基因。miR-23a 的过表达显著抑制了 XIAP 的表达。XIAP 的敲低也诱导了滋养细胞凋亡。此外，XIAP 表达的恢复显著消除了 miR-23 过表达诱导的滋养细胞凋亡。综上所述，我们的研究表明，miR-23a 通过抑制 XIAP 诱导滋养细胞凋亡，这可能与子痫前期有关。我们的研究结果为理解子痫前期的发病机制提供了新的见解，并为子痫前期提供了一个潜在的治疗靶点。
