Impaired mitophagy is involved in the trophoblastic excessive apoptosis in preeclampsia caused by ROS

Zhou Xiaobo; Shi Shuming; Zhang Hua

doi:10.13406/j.cnki.cyxb.001218

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Impaired mitophagy is involved in the trophoblastic excessive apoptosis in preeclampsia caused by ROS

更新时间：2024-01-17

- Impaired mitophagy is involved in the trophoblastic excessive apoptosis in preeclampsia caused by ROS
- Journal of Chongqing Medical University Vol. 42, Issue 3, Pages: 315-318(2017)
- 作者机构：
  
  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
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.001218
  CLC： R714.244
- Published：2017，
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Zhou Xiaobo, Shi Shuming, Zhang Hua. Impaired mitophagy is involved in the trophoblastic excessive apoptosis in preeclampsia caused by ROS. [J]. Journal of Chongqing Medical University 42(3):315-318(2017)
DOI：

Zhou Xiaobo, Shi Shuming, Zhang Hua. Impaired mitophagy is involved in the trophoblastic excessive apoptosis in preeclampsia caused by ROS. [J]. Journal of Chongqing Medical University 42(3):315-318(2017) DOI： 10.13406/j.cnki.cyxb.001218.

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

Objective:To characterize the expression of BCL2/adenovirus E1 B 19 k D protein-interacting protein 3（BNIP3）in placenta and mitophagy induced by BNIP3 in regulation of apoptosis in preeclampsia. Methods:The expressions of BNIP3 and cleaved-caspase3 protein were detected in placenta from normal pregnancies and pregnancies complicated with preeclampsia by Western blot.HTR8/SVneo were used as the preeclampsia cell model and treated with hypoxia/reoxygenation（H/R）. RNA interference technology was performed by using BNIP3 specific small interfering RNA（si RNA）;Western blot was used to identify the expression of BNIP3 after RNA interference. The experiments were divided into two groups:si-NC group and si-BNIP3 group

then treated with H/R

the production of reactive oxygen species（ROS）within cells was detected by 2’

7’-dichlorodi-hydro-fluorescein diacetate（DCFH-DA）and flow cytometry was used to detect the apoptotic cells. Results:The expression of BNIP3 in placenta from preeclampsia was lower and the expression of cleaved-caspase3 was higher（P=0.015

P=0.019）. Within the preeclampsia cell model

the knock-down of BNIP3 by si RNA significantly increased the production of ROS and activities of apoptosis in HTR8/SVneo（P=0.022

P=0.038）. Conclusion:Impaired mitophagy induced by BNIP3 within placenta participates in the excessive production of ROS and excessive apoptosis.

关键词

线粒体自噬子痫前期活性氧凋亡

Keywords

mitophagypreeclampsiareactive oxygen speciesapoptosis

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