Department of Obstetrics, the Affiliated Hospital of Qingdao University, 16 Jiangsu Road, 266000, Qingdao, China.
Department of Obstetrics, the Weifang Yidu Central Hospital, Weifang, China.
Reprod Biol Endocrinol. 2022 Feb 24;20(1):38. doi: 10.1186/s12958-022-00909-2.
Preeclampsia (PE), a pregnancy disorder that affects 5-7% of pregnant women, is among the primary causes for maternal and perinatal mortality. PE is believed to be associated with insufficient invasion of villous and extravillous trophoblasts (EVTs), which hampers uterine spiral artery remodeling and finally induces PE. But the mechanism responsible for reduction of trophoblast invasion remains unclear. In this study, placental tissues taken from healthy donors and PE patients were used to evaluate the miR-326 expression; CCK8 and colony formation assays were used to confirm the effect of miR-326 on cell proliferation; transwell assay was used to demonstrate the effect of miR-326 on cell invasion capability; western blot was used to investigate the underlying mechanism; and luciferase assay was used to detect the effect of miR-326 on YAP/TAZ-mediated transcription activity. It was revealed the miR-326 expression was higher in placentas from PE patients than from healthy donors. After transfection of miR-326 mimics, trophoblast proliferation and invasion were impaired. Using TargetScan, we speculated that PAX8 was a target of miR-326, which was later confirmed by western blot. The YAP/TAZ expression was also downregulated after transfection with miR-326. Luciferase assay demonstrated that overexpression of miR-326 suppressed YAP/TAZ-mediated transcription activity by targeting PAX8. Overexpression of PAX8 could partly rescue miR-326-induced suppression of trophoblast proliferation and invasion. Taken together, our result indicated that miR-326 suppresses trophoblast growth, invasion, and migration by means of targeting PAX8 via the Hippo pathway.
子痫前期(PE)是一种妊娠疾病,影响 5-7%的孕妇,是孕产妇和围产儿死亡的主要原因之一。PE 被认为与绒毛和绒毛外滋养细胞(EVT)的侵袭不足有关,这阻碍了子宫螺旋动脉重塑,最终导致 PE。但是,导致滋养细胞侵袭减少的机制尚不清楚。在这项研究中,使用来自健康供体和 PE 患者的胎盘组织来评估 miR-326 的表达;使用 CCK8 和集落形成测定来确认 miR-326 对细胞增殖的影响;使用 Transwell 测定来证明 miR-326 对细胞侵袭能力的影响;使用 Western blot 来研究潜在的机制;使用荧光素酶测定来检测 miR-326 对 YAP/TAZ 介导的转录活性的影响。结果表明,PE 患者胎盘组织中的 miR-326 表达高于健康供体。转染 miR-326 模拟物后,滋养细胞增殖和侵袭受损。使用 TargetScan,我们推测 PAX8 是 miR-326 的靶标,这后来通过 Western blot 得到证实。转染 miR-326 后,YAP/TAZ 的表达也下调。荧光素酶测定表明,过表达 miR-326 通过靶向 PAX8 抑制 YAP/TAZ 介导的转录活性。过表达 PAX8 可以部分挽救 miR-326 诱导的滋养细胞增殖和侵袭抑制。总之,我们的结果表明,miR-326 通过 Hippo 通路靶向 PAX8 抑制滋养细胞的生长、侵袭和迁移。