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作 者:郑志伟[1,2] 劳海燕[2] 余细勇[2,3] 陈纪言[3] 林秋雄[2] 麦丽萍[2] 钟诗龙[2,3]
机构地区:[1]南方医科大学药学院,广东广州510515 [2]广东省人民医院医学研究中心 [3]广东省心血管病研究所,广东广州510080
出 处:《中国病理生理杂志》2011年第12期2313-2317,共5页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.81072701);广东省自然科学基金资助项目(No.10151008002000002)
摘 要:目的:检测血浆循环miR-126和miR-16在冠心病患者和健康人群血浆中的表达,进一步探讨miR-126对血管内皮细胞的影响。方法:(1)收集52例冠心病心肌梗死型患者和52例健康人群的血样标本,采用Trizol LS提取血浆中总RNA,检测血浆miR-126和miR-16的表达;(2)通过转染在人血管内皮细胞株EA.hy926中抑制miR-126的表达,转染30 h后检测血管内皮生长因子的表达。结果:(1)与健康人群相比,循环miR-126在冠心病患者中的表达显著下降(P<0.05);miR-16在两组间的表达无显著差异(P>0.05);(2)内皮细胞株EA.hy926中miR-126被抑制后,血管内皮生长因子的表达为对照组的2.08倍(P<0.05)。结论:血浆循环miR-126在冠心病患者表达下降,血浆循环miR-16在人群中的表达较稳定;miR-126通过负性调节血管内皮生长因子的表达,对血管内皮细胞产生调节作用。AIM: To investigate the role of plasma circulating miR-126 and miR-16 in the patients with coronary artery heart disease and to explore the influence of miR-126 on vascular endothelial cells.METHODS: Plasma total RNA was isolated from 52 patients with stable coronary artery disease and 52 healthy volunteers.The circulating miR-126 and miR-16 in those people were detected using specific primers.Endothelial cell line EA.hy926 was transfected with a miR-126 inhibitor,and total RNA of the cells was isolated 30 h after transfection to detect the expression level of vascular endothelial growth factor(VEGF).RESULTS: The expression of plasma circulating miR-126 was significantly decreased in the patients with coronary artery heart disease compared with healthy controls(P0.05).No significant difference of circulating miR-16 between the patients with coronary artery heart disease and healthy controls was observed(P0.05).The expression of VEGF in the endothelial cell line EA.hy926 transfected with miR-126 inhibitor was 2.08 times higher than that in negative control cells 30 h after transfection(P0.05).CONCLUSION: Plasma circulating miR-126 is significantly decreased in the patients with coronary artery heart disease.Plasma circulating miR-16 in the patients with coronary artery heart disease and in the healthy controls is stable.miR-126 negatively regulates the expression of VEGF in vascular endothelial cells.
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