...
首页> 外文期刊>European review for medical and pharmacological sciences. >MiR-200c regulates apoptosis of placental trophoblasts in preeclampsia rats through Wnt/β-catenin signaling pathway
【24h】

MiR-200c regulates apoptosis of placental trophoblasts in preeclampsia rats through Wnt/β-catenin signaling pathway

机译:miR-200c通过Wnt /β-catenin信号传导途径调节胎盘大鼠胎盘滋养细胞的凋亡

获取原文
   

获取外文期刊封面封底 >>

       

摘要

OBJECTIVE: To investigate the influence of micro ribonucleic acid 200c (miR-200c) on the apoptosis of placental trophoblasts in a rat model of preeclampsia (PE). MATERIALS AND METHODS: PE model in rats was established for extracting placental trophoblasts. Overexpression or knockdown of miR-200c was achieved by transfection of miR-200c mimics or inhibitor. Flow cytometry was carried out to detect the apoptotic rate of placental trophoblasts. Dual-luciferase reporter gene assay was performed to detect the interaction of miR-200c with WNT1. Western blotting was applied to determine the changes of protein levels in placental trophoblasts. RESULTS: The expression level of miR-200c in placental trophoblasts of PE group was significantly higher than that in control group. The apoptosis rate was (22.45 ± 2.62)%, (6.58 ± 1.28)%, and (9.57 ± 1.35)% in miR-200c mimic group, miR-200c inhibitor group, and control group, respectively, showing statistically significant differences. MiR-200c overexpression downregulated the expression level of anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), but upregulated expression levels of apoptotic proteins Bcl-2-associated X protein (Bax) and active Caspase-3. MiR-200c suppressed WNT1 expression through the interaction with the 3’-untranslated region (3’-UTR) of WNT1. The expressions of WNT1 and β-catenin were up-regulated after miR-200c overexpression, which was reversed by the Wnt/β-catenin pathway activator. CONCLUSIONS: MiR-200c is involved in the development and progression of PE through the Wnt/β-catenin signaling pathway.
机译:目的:探讨微核糖核酸200C(miR-200c)对预口度(PE)大鼠胎盘性滋养细胞凋亡的影响。材料和方法:建立大鼠的体育型模型用于提取胎盘滋养细胞。通过转染miR-200c模拟剂或抑制剂来实现miR-200c的过度表达或敲低。进行流式细胞术以检测胎盘滋养细胞的凋亡率。进行双荧光素酶报告器基因测定以检测miR-200c与wnt1的相互作用。施用蛋白质印迹以确定胎盘性滋养细胞中蛋白质水平的变化。结果:PE组胎盘滋养细胞中miR-200c的表达水平显着高于对照组。细胞凋亡率分别为(22.45±2.62)%,(6.58±1.28)%,(6.58±1.28)%,分别显示miR-200c模拟基团,miR-200c抑制剂组和对照组的(9.57±1.35)%,显示出统计学上显着的差异。 miR-200c过表达下调了抗凋亡蛋白B细胞淋巴瘤2(bcl-2)的表达水平,但是凋亡蛋白Bcl-2相关X蛋白(Bax)和活性Caspase-3的上调表达水平。 miR-200c通过与Wnt1的3'-wonsterralated区域(3'-UTR)的相互作用来抑制WNT1表达。在MiR-200C过表达后,Wnt1和β-catenin的表达是上调的,其被Wnt /β-catenin途径活化剂反转。结论:MIR-200C通过WNT /β-Catenin信号传导途径参与PE的开发和进展。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号