摘要
目的:探讨miR-21反义寡核苷酸(AS-miR-21)对内皮型一氧化氮合酶(eNOS)基因调节的分子机制及血管内皮细胞增殖相关转录因子AP1作用机制的可能性。方法:应用MTT方法检测细胞增殖抑制率;细胞划痕实验检测细胞迁移能力;Transwell侵袭小室模型分别检测各组细胞侵袭能力的变化;Western blot检测miR-21表达相关情况及细胞核转录因子eNOS和AP1表达情况。结果:AS-miR-21能抑制人脐静脉内皮细胞(HUVECs)生长,促进其凋亡;AS-miR-21对HUVECs迁移和侵袭具有抑制作用;AS-miR-21干预下HUVECs的eNOS和AP1蛋白表达明显减少。结论:AS-miR-21显著抑制eNOS和AP1蛋白表达,转录因子AP1在ASmiR-21对eNOS的表达调节中起重要作用。
Objective：To investigate miR-21 antisense oligonucleotide regulates expression of the human endothelial nitric oxide synthase gene and proliferation of endothelial cells by a mechanism related to the transcription factor AP1.Method：MTT was used to measure inhibition in cultured HUVECs.Migration ability of HUVECs was measured by scratch wound model in vitro.The protein expression of AP1 and eNOS were examined by Western blot.Result：MiR-21 antisense oligonucleotide inhibited the HUVECs proliferation and induced apoptosis.MiR-21 antisense oligonucleotide decreased cell migration in HUVECs.MiR-21 antisense oligonucleotide regulated AP1 and eNOS protein expression was significantly decreased.Conclusion：MiR-21 antisense oligonucleotide suppresses eNOS expression and AP1 expression in HUVECs.Meanwhile,miR-21 antisense oligonucleotide regulated expression of the eNOS by the target AP1.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2014年第10期900-902,共3页
Journal of Clinical Cardiology
基金
国家自然科学基金(No:81373403)
广西硕士研究生科研创新项目(No:YCSZ2013031)
