miR-34a-5p靶向Smad4抑制子宫内膜纤维化的机制研究

被引：1
|
作者：
范李静
张苗
郑瑛红
刘文杰
范小斌
机构：
[1] 西北大学附属医院西安市第三医院妇产科
来源：
现代妇产科进展 | 2022年 / 31卷 / 09期
关键词：
miR-34a-5p; 宫腔粘连; 纤维化; Smad4;
D O I：
10.13283/j.cnki.xdfckjz.2022.09.005
中图分类号：
R711 [妇科学];
学科分类号：
摘要：
目的:探讨miR-34a-5p在子宫内膜纤维化中的作用及机制。方法:收集正常及宫腔粘连患者的子宫内膜组织，实时定量PCR检测子宫内膜组织中miR-34a-5p表达水平。子宫内膜间质细胞(hESC)转染miR-34a-5p mimics(或mimics对照)或Smad4过表达质粒，并用转化生长因子-β1(TGF-β1)处理。CCK-8检测细胞增殖能力。实时定量PCR和Western blot法检测纤维化标志物α-平滑肌肌动蛋白(α-SMA)、纤维连接蛋白(FN)和胶原蛋白Ⅰ(COL1A1)的mRNA和蛋白表达水平。生物信息学软件预测miR-34a-5p的靶基因并用双荧光素酶报告基因方法验证。结果:与正常患者相比，宫腔粘连患者子宫内膜组织中miR-34a-5p水平降低。TGF-β1处理后可显著降低hESC细胞中miR-34a-5p水平，增加细胞增殖率。与阴性对照NC相比，转染miR-34a-5p mimics可显著降低hESC细胞的增殖率，以及α-SMA、FN和COL1A1的mRNA和蛋白表达水平。Smad4经鉴定是miR-34a-5p的靶基因。过表达Smad4可逆转miR-34a-5p mimics抗增殖及抗纤维化作用，表现为hESC细胞增殖率增加，α-SMA和COL1A1表达水平增加。结论:miR-34a-5p通过下调Smad4抑制TGF-β1诱导的hESC细胞增殖和纤维化。
引用
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页码：678 / 682
页数：5
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