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Anti-miR-21与血管紧张素II对血管内皮细胞eNOS基因表达及细胞增殖的协同调节作用

  • 莫国君,欧和生

* 通信作者: 欧和生, 单位:广西医科大学药理学教研室 530021

摘要

[摘要]
目的:探讨miR-21抑制剂(Anti-miR-21)是否抑制血管紧张素II(AngII)参与内皮型一氧化氮合酶(eNOS)表达的调控及其对血管内皮细胞增殖的影响。

方法:本研究将anti-miR-21导入经血管紧张素II诱导的人脐静脉内皮细胞(HUVECs),观测anti-miR-21和血管紧张素II对eNOS表达及HUVECs增殖的影响。用四甲基偶氮唑蓝(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;RT-PCR和Western blotting检测转录因子AP1与eNOS mRNA和蛋白表达水平。

结果:AngII能促进血管内皮细胞的增殖和迁移,Anti-miR-21对其效果皆具有抑制作用,AngII刺激下HUVECs的AP1与eNOS mRNA和蛋白表达均增加,转染anti-miR-21对其mRNA和蛋白表达都起到抑制作用。

结论:Anti-miR-21明显抑制AngII刺激下HUVECs的增殖及eNOS的表达;AP1在AngII刺激下HUVECs的eNOS表达中起关键的调控作用。

关键词:[关键词]Anti-miR-21; 血管紧张素II; 一氧化氮合酶; AP1转录因子

ABSTRACT

[ABSTRACT]To investigate whether anti-miR-21 collaborative angiotensin II (AngII) is involved in the regulation of endothelial nitric oxide synthase (eNOS) expression and vascular endothelial cell proliferation..METHODS: anti-miR-21 was transfected into the human umbilical vein endothelial cells ( HUVECs) by angiotensin II induced. The cell proliferation was detected by MTT assay.The cell migration was detected by scratch wound model in vitro. The expression of eNOS and Sp1 at mRNA and protein levels was examined by real-time PCR and Western blotting. RESULTS:AngII significantly promoted vascular endothelial cell proliferation and migration,anti-miR-21 inhibited its effect. AngII increased the expression of AP1 and eNOS at mRNA and protein levels. anti-miR-21 inhibited the effect of AngII on HUVECs.CONCLUSION: Anti-miR-21 significantly suppresses the effect of angiotensin II on proliferation of HUVECs and the eNOS expression. AP1 acts as one of the important factors in the regulation of eNOS expression by Anti-miR-21.

Key words: [KEY WORDS]Anti-miR-21; Angiotensin II; Nitric oxide; AP1 transcription factor

引用本文 / How to Cite This Article

莫国君,欧和生.Anti-miR-21与血管紧张素II对血管内皮细胞eNOS基因表达及细胞增殖的协同调节作用 [J]. 国际精神病学杂志, 2017, 34(5): 681-684

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