摘要
目的:观察肌细胞增强因子2A(MEF2A)RNA干扰对小鼠主动脉内皮细胞MEF2A及细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)表达的影响。方法:培养小鼠主动脉内皮细胞,构建MEF2A RNA干扰慢病毒或者阴性对照慢病毒(NC)并转染小鼠主动脉内皮细胞。实验设对照组(不加慢病毒)、NC组和MEF2A RNA干扰组3组,应用ELISA和RT-PCR法分别检测MEF2A及ICAM-1、VCAM-1蛋白及mRNA的表达水平。结果:ICAM-1在对照组、NC组和MEF2A RNA干扰组上清液中的表达量分别为(1.133±0.182)、(1.267±0.115)、(2.249±0.185)μg/L;VCAM-1在对照组、NC组和MEF2A RNA干扰组上清液中的表达量分别为(2.382±0.204)、(2.253±0.281)、(5.077±0.198)μg/L。ICAM-1、VCAM-1在上清液中的水平及mRNA表达水平,NC组与对照组相比,差异无统计学意义(P>0.05);MEF2A RNA干扰组与对照组和NC组相比均升高(P<0.05)。结论:慢病毒介导的MEF2A RNA干扰可抑制小鼠主动脉内皮细胞MEF2A活性及mRNA的表达,并可促进血管内ICAM-1、VCAM-1蛋白及mRNA的表达。
Aim： To identify the effects of RNA interference of myocyte enhancer factor 2A（ MEF2A） on the expressions of MEF2 A and relative inflammatory genes ICAM-1 and VCAM-1 in mice aortic endothelial cells. Methods： The aortic endothelial cells in mice were cultivated,then MEF2 A lentivirus RNA interference or negative control lentivirus（ NC）were built and transfected aortic endothelial cells in mice. The cells were allocated into control group（ without lentivirus）,NC group,and MEF2 A RNA interference group. MEF2 A,ICAM-1,and VCAM-1 expressions were detected by ELISA,and mRNA levels of MEF2 A,ICAM-1,and VCAM-1 were further examined by RT-PCR. Results： In the control group,NC group,and MEF2 A RNA interference group,ICAM-1 expression in the supernatant fluid were（ 1. 133 ± 0. 182）,（ 1. 267 ± 0. 115）,and（ 2. 249 ± 0. 185） μg/L,VCAM-1 expression in the supernatant fluid were（ 2. 382 ± 0. 204）,（ 2. 253 ± 0. 281）,and（ 5. 077 ± 0. 198） μg/L. There was no significant difference in ICAM-1 or VCAM-1 expression in the supernatant fluid between NC group and the control group（ P 0. 05）. When MEF2 A RNA interference group was compared with the control group and NC group,there were significant differences（ P 0. 05）. Conclusion： Lentivirus-mediated RNA interference of MEF2 A could inhibit the expression of MEF2 A and promote intravascular ICAM-1,VCAM-1 activity mRNA expression.
出处
《郑州大学学报（医学版）》
CAS
北大核心
2016年第4期502-505,共4页
Journal of Zhengzhou University(Medical Sciences)
基金
河南省高校科技创新团队基金资助项目14IRTSTHN018
