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目的:探讨类固醇受体辅助活化因子-3(steroid receptor coactivator-3,SRC-3)参与人脐静脉内皮细胞株(HUVECs)受损的信号通路,及其在子痫前期发病机制中的作用。方法:收集2014年10月至2015年10月在重庆医科大学附属第一医院行选择性剖宫产手术的正常足月妊娠组(31例)以及子痫前期组(29例)的胎盘组织。使用Western blot检测2组胎盘组织SRC-3的表达。脐静脉内皮细胞株(HUVECs)分为4个处理组:正常常氧对照(N)培养组、缺氧/复氧(H/R)培养组、SRC-3 sh RNA慢病毒敲降(sh SRC-3)培养组以及PI3K特异性抑制剂(LY294002)培养组。使用Western blot检测内皮细胞中SRC-3、p-Akt(Ser473)、Akt、p-m TOR(Ser2481)、m TOR的表达。使用细胞管腔成型实验检测内皮细胞血管形成能力。结果:SRC-3在子痫前期胎盘组织蛋白水平低于正常足月胎盘(t=3.501,P=0.013)。细胞学实验中,与N组相比,H/R组、sh SRC-3组及LY294002组HUVECs的SRC-3(t=4.236,P=0.007;t=5.469,P=0.002;t=4.165,P=0.008)、p-Akt(Ser473)/Akt(t=5.214,P=0.002;t=5.188,P=0.002;t=7.054,P=0.000)、p-m TOR(Ser2481)/m TOR(t=4.832,P=0.003;t=5.695,P=0.001;t=5.699,P=0.001)表达降低。H/R组、sh SRC-3组、LY294002组HUVECs血管形成能力低于N组(t=5.268,P=0.002;t=4.648,P=0.004;t=4.087,P=0.009)。结论:SRC-3可能通过PI3K/Akt/m TOR通路参与子痫前期的发病机制。
OBJECTIVE: To investigate the signaling pathway implicated in steroid receptor coactivator-3 (SRC-3) in human umbilical vein endothelial cell line (HUVECs) and its role in the pathogenesis of preeclampsia. Methods: The placenta tissues of normal term pregnancy group (31 cases) and preeclampsia group (29 cases) undergoing elective cesarean section at the First Affiliated Hospital of Chongqing Medical University from October 2014 to October 2015 were collected. Western blot was used to detect the expression of SRC-3 in two groups of placenta. HUVECs were divided into four groups: normal normoxic (N) group, hypoxia / reoxygenation group (H / R) group, SRC-3 sh RNA lentivirus knockdown -3) culture group and PI3K-specific inhibitor (LY294002) culture group. Western blot was used to detect the expression of SRC-3, p-Akt (Ser473), Akt, p-m TOR (Ser2481) and mTOR in endothelial cells. Endothelial cell vascularization was measured using a cell lumen assay. Results: The placental protein level of SRC-3 in preeclampsia was lower than that of normal full-term placenta (t = 3.501, P = 0.013). Cytology experiments showed that SRC-3 (t = 4.236, P = 0.007; t = 5.469, P = 0.002; t = 4.165, P = 0.008), p-Akt (Ser473) / Akt (t = 5.214, P = 0.002; t = 5.188, P = 0.002; 4.832, P = 0.003; t = 5.695, P = 0.001; t = 5.699, P = 0.001). HUVECs in H / R group, sh SRC-3 group and LY294002 group had less vascularity than those in N group (t = 5.268, P = 0.002; t = 4.648, P = 0.004; t = 4.087, P = 0.009). Conclusion: SRC-3 may participate in the pathogenesis of preeclampsia through PI3K / Akt / m TOR pathway.