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miR-101通过调控内质网蛋白44调节子痫前期内质网应激诱导的滋养细胞凋亡 被引量:1

MiR-101 regulates apoptosis of trophoblast cells in preeclampsia by targeting endoplasmic reticulum (ER) protein 44 through endoplasmic reticulum stress
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摘要 目的:探讨人类子痫前期(PE)中miR-101介导的内质网蛋白44(ERp44)对滋养细胞凋亡和内质网应激过程的调控。方法:采用实时定量聚合酶链反应(qPCR)检测25例PE和25例正常孕妇胎盘组织中miR-101的表达水平,分析ERp44与miR-101表达的相关性。分别过表达和封闭miR-101表达后,采用Western blot法检测ERp44的表达,采用流式细胞技术检测滋养细胞的凋亡数量改变,采用Western blot法检测内质网应激相关的凋亡蛋白的表达情况。结果:(1)PE胎盘中miR-101表达下调,低于正常妊娠组的25%(P<0.05);miR-101表达与ERp44呈显著负相关(Pearson相关系数=-0.826,P<0.01);(2)滋养细胞HTR-8/SVneo中过表达miR-101后,ERp44表达下调约50%(P<0.01);封闭miR-101表达后,ERp44表达升高2.39倍(P<0.01);(3)过表达miR-101,细胞凋亡数量减少,同时通过靶向结合ERp44而抑制内质网应激诱导的凋亡蛋白反应;封闭miR-101表达,细胞凋亡数量增加,内质网应激诱导的凋亡蛋白反应增加。结论:PE中miR-101通过靶向调节ERp44参与内质网应激诱导的滋养细胞凋亡过程。 Objective: To investigate the possible association between miR-101 and apoptosis of human trophoblast cells mediated by endoplasmic reticulum protein 44( ERp44) through endoplasmic reticulum stress in preeclampsia.Methods: We explored the expression of miR-101 in preeclampsia placentas( n = 25) compared with normotensive pregnant placentas( n=25).The correlation between miR-101 and ERp44 was also analyzed.The apoptotic rate of trophoblast cells and ER stress induced apoptotic proteins were assayed when the HTR-8 / SVneo cells were treated with miR-101 mimics or inhibitors in vitro.Results:( 1) We found a 25% lower expression of miR-101( P<0.05) and the inverse correlation was-0.826 between miR-101 and ERp44 protein in preeclamptic placentas( P < 0.01).( 2) Upregulation of miR-101 expression could reduce expression of ERp44 protein while a down-regulation of miR-101 promote ERp44 protein expression by 2. 39-fold.( 3) Upregulation of miR-101 expression could inhibit trophoblast cells HTR-8 / SVneo apoptosis and repress ER stress induced apoptotic proteins by targeting ERp44 in vitro while inhibition of miR-101 could induce HTR-8 / SVneo cells apoptosis.Our findings indicated that overexpression of miR-101 could down-regulate ERp44 and suppress apoptosis in trophoblast cells during preeclampsia.Conclusion: miR-101 can contribute to ER stress induced trophoblast cells apoptosis by targeting ERp44 in preeclampsia.
作者 邹艳芬 姜子燕 左青 孙丽洲 Zou Yanfen;Jiang Ziyan;Zuo Qingl;Department of Obstetrics and Gynecology,The First Affiliated Hospital of Nanjing Medical University;
出处 《现代妇产科进展》 CSCD 2014年第3期198-202,共5页 Current Advances In Obstetrics and Gynecology
基金 国家自然科学基金(No:81070511)
关键词 子痫前期 miR-101 内质网蛋白44(ERp44) 内质网应激 滋养细胞HTR-8/SVneo 凋亡 Preeclampsia miR-101 Endoplasmic reticulum chaperone protein 44(ERp44) Endoplasmic reticulum(ER) stress Trophoblast cells HTR-8/SVneo Apoptosis
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