线粒体自噬受损引起的ROS清除障碍导致子痫前期患者滋养细胞过度凋亡

发布时间：2018-04-17 22:42

  本文选题：线粒体自噬 + 子痫前期　； 参考：《重庆医科大学学报》2017年03期

【摘要】：目的:探讨胎盘组织中Bcl-2家族的前凋亡因子—腺病毒E1B19 k D相互作用蛋白3(BCL2/adenovirus E1B 19 k D protein-interacting protein 3,BNIP3)的表达及其介导的线粒体自噬在子痫前期(preeclampsia,PE)胎盘滋养细胞凋亡调控中的作用。方法:应用Western blot方法检测BNIP3和cleaved-caspase3在对照及PE胎盘中的表达差异。以人绒毛外滋养细胞株HTR8/SVneo通过缺氧/复氧(hypoxia/reoxygenation,H/R)构建PE细胞模型。构建BNIP3小干扰RNA,转染细胞后,H/R处理各组细胞,DCFH-DA法检测各组细胞活性氧(reactive oxygen species,ROS)生成,流式细胞仪检测细胞凋亡。结果:与正常胎盘相比,在PE胎盘组织中BNIP3表达明显降低(P=0.015),而凋亡蛋白cleaved-caspase3明显增加(P=0.019);在PE细胞模型中,BNIP3敲低组较对照组的ROS产量显著增加(P=0.022),且凋亡增加(P=0.038)。结论:BNIP3介导的线粒体自噬不足引起ROS清除障碍可能参与PE胎盘滋养细胞过度凋亡的发生。
[Abstract]:Aim: to investigate the expression of proapoptotic factor-adenovirus E1B19 kD interaction protein 3(BCL2/adenovirus E1B 19 KD protein-interacting protein 3 in placental tissues and the role of mitochondrial autophagy in the regulation of placental trophoblast apoptosis.Methods: Western blot method was used to detect the expression of BNIP3 and cleaved-caspase3 in the control group and PE placenta.The PE cell model was established by hypoxia / reoxygenation H / R with human extracellular trophoblastic cell line HTR8/SVneo.BNIP3 small interfering RNAs were constructed and treated with H / R after transfection. The production of reactive oxygen species-ROSs in each group was detected by DCFH-DA and apoptosis was detected by flow cytometry.Results: compared with the normal placenta, the expression of BNIP3 decreased significantly in the placenta of PE, while the apoptotic protein cleaved-caspase3 increased significantly, and the ROS production in the low knock group of PNIP3 in PE cell model was significantly higher than that in the control group.Conclusion the dysfunction of ROS clearance induced by mitochondrial autophagy induced by 10% BNIP3 may be involved in the excessive apoptosis of PE placental trophoblastic cells.
【作者单位】： 重庆医科大学附属第一医院产科重庆医科大学中国-加拿大-新西兰联合母胎医学实验室;
【基金】：国家自然科学基金面上资助项目(编号:81370732)
【分类号】：R714.244
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本文编号：1765656