微小RNA-101及髓细胞白血病因子-1在子痫前期中的表达及对胎盘滋养层细胞的影响  

Expression of MicroRNA-101 and Myeloid Cell Leukemia-1 in Preeclampsia and Their Effects on Placental Trophoblast Cells

作　　者：乔小改[1] 蔡大军[1] 张庆[1] QIAO Xiaogai;CAI Dajun;ZHANG Qing(Department of Obstetrics and Gyn ecology,The Second Affiliated Hospital of Zhengzhou University,Zhe ngzhou Henan 450000,China)

机构地区：[1]郑州大学第二附属医院妇产科,河南郑州450000

出　　处：《实用妇产科杂志》2022年第10期774-778,共5页Journal of Practical Obstetrics and Gynecology

基　　金：河南省医学科技攻关计划项目(编号:201702091)。

摘　　要：目的:探讨微小RNA-101(miR-101)和髓细胞白血病因子-1(MCL1)在子痫前期(PE)中的表达及对胎盘滋养层细胞增殖、凋亡及侵袭的影响。方法:收集2018年6月至2020年12月在郑州大学第二附属医院妇产科就诊的56例PE孕妇(PE组)和60例正常孕妇(对照组)的相关资料,采用荧光定量PCR(qRT-PCR)检测其胎盘组织中miR-101的相对表达水平,蛋白免疫印迹法及免疫组织化学法检测MCL1的表达,分析二者表达的相关性;采用双荧光素酶报告基因实验验证人滋养层细胞HTR8/SVneo中miR-101与MCL1的靶向关系;通过转染分别抑制HTR8/SVneo细胞中miR-101和MCL1的表达,并采用CCK8法、流式细胞仪及细胞侵袭实验检测细胞增殖、凋亡及侵袭能力的变化。结果:PE组胎盘组织中miR-101水平明显高于对照组,MCL1蛋白水平明显低于对照组(P<0.05),且二者表达呈负相关(r<0,P<0.05);miR-101与MCL1之间存在靶向关系,体外抑制miR-101后HTR8/SVneo细胞的增殖和侵袭活性升高,凋亡率下降(P<0.05),与单独抑制miR-101相比,共抑制miR-101和MCL1的表达后细胞的增殖和迁移能力降低,凋亡率升高(P<0.05)。结论:miR-101在PE胎盘组织中高表达,并通过靶向MCL1引起滋养层细胞增殖、浸润不足和异常凋亡,参与PE的发生进展。Objective:To investigate the expression of microRNA-101(miR-101)and myeloid cell leukemia-1(MCL1)in preeclampsia(PE),and its effects on the proliferation,apoptosis and invasion of placental trophoblast cells.Methods:The relative information of 56 pregnant women with PE(PE group)and 60 normal pregnant women(control group)who visited the Department of Gynecology and Obstetrics of The Second Affiliated Hospital of Zhengzhou University from June 2018 to December 2020 were collected.Fluorescence quantitative PCR was used to detect the relative expression level of miR-101 in their placental tissues,and Western blot was used to detect the expression level of MCL1,and the correlation between the expression of the miR-101 and MCL1.Dual luciferase reporter gene assay was used to verify the targeting relationship between miR-101 and MCL1 in human trophoblast cells HTR8/SVneo.The expression of miR-101 and MCL1 in HTR8/SVneo cells was inhibited by transfection,and the changes of cell proliferation,apoptosis and invasion ability were detected by CCK8 assay,flow cytometry and cell invasion assay.Results:The level of miR-101 in the placenta tissue of PE group was significantly higher than that of the control group,while the level of MCL1 protein was significantly lower than that of the control group(P<0.05),and the levels of the two were negatively correlated(r<0,P<0.05).There was a targeting relationship between miR-101 and MCL1.Inhibition of miR-101 in vitro increased the proliferation and invasion activity of HTR8/SVneo cells,and decreased the apoptosis rate(P<0.05).Compared with the inhibition of miR-101 alone,the proliferation and migration ability of cells were decreased and the apoptosis rate was increased after co-inhibition of miR-101 and MCL1 expression(P<0.05).Conclusions:MiR-101 is highly expressed in PE placental tissues,and participates in the occurrence and progression of PE by targeting MCL1 to induce proliferation,insufficient infiltration and abnormal apoptosis of trophoblast cells.

关 键 词：微小RNA-101 髓细胞白血病因子-1 子痫前期 滋养层细胞 

分 类 号：R714.244[医药卫生—妇产科学]