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miR-21抑制剂对血管紧张素Ⅱ诱导人脐静脉内皮细胞增殖及eNOS表达的影响

Effects of miR-21 inhibitor on angiotensinⅡ-induced human umbilical vein endothelial cells proliferation and eNOS expression
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摘要 目的:探讨miR-21抑制剂对血管紧张素Ⅱ(AngⅡ)诱导人脐静脉内皮细胞(HUVECs)增殖及内皮型一氧化氮合酶(eNOS)表达的影响。方法:将miR-21抑制剂转染至经AngⅡ诱导的HUVECs,采用MTT法检测细胞的增殖情况,细胞划痕实验检测细胞迁移能力,分别采用RT-PCR和western blotting法检测转录因子AP1和eNOS的mRNA和蛋白表达水平。结果:AngⅡ能促进HUVECs增殖和迁移,并使细胞中AP1、eNOS mRNA和蛋白表达明显上调(P<0.05);miR-21抑制剂转染细胞后,AngⅡ促进HUVECs增殖和迁移的作用发生显著逆转(P<0.05),且AP1、eNOS mRNA和蛋白表达明显下调(P<0.05)。结论:miR-21抑制剂能够抑制AngⅡ刺激下HUVECs的增殖及eNOS的表达;AP1在AngⅡ诱导细胞eNOS表达中可能起到关键的调控作用。 Objective:To investigate the effects of miR-21 inhibitor on angiotensin Ⅱ (Ang Ⅱ ) induced human umbilical vein endothelial cells (HUVECs) proliferation and the expression of endothelial nitric oxide synthase (eNOS). Methods: miR-2 inhibitor was transfected into the Ang Ⅱ induced HUVECs. The cell proliferation and migration were detected by MTT assay and wound healing assay, respectively. The expression of AP1 and eNOS were determined by RT-PCR and western blotting. Results: Ang Ⅱ could significantly promote the HUVECs proliferation and migration, and up-regulate the AP1 and eNOS expres- sions ( P 〈0.05). However, the effects of Ang Ⅱ were reversed by miR-21 inhibitor. Conclusion: miR-21 inhibitor could suppress Ang Ⅱ-induced HUVECs proliferation and eNOS expression. AP1 might be one of the key factors in the regulation of eNOS expression.
机构地区 广西医科大学
出处 《广西医科大学学报》 CAS 2017年第5期681-684,共4页 Journal of Guangxi Medical University
基金 国家自然科学基金资助项目(No.81373403)
关键词 miR-21抑制剂 血管紧张素Ⅱ 一氧化氮合酶 AP1转录因子 miR-21 angiotensin Ⅱ nitric oxide synthase AP1 transcription factor
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