首页> 中文期刊>郑州大学学报(医学版) >MEF2A RNA 干扰对小鼠主动脉内皮细胞 MEF2A 表达及细胞间黏附分子-1、血管细胞黏附分子-1表达的影响

MEF2A RNA 干扰对小鼠主动脉内皮细胞 MEF2A 表达及细胞间黏附分子-1、血管细胞黏附分子-1表达的影响

     

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 expres-sions of MEF2A and relative inflammatory genes ICAM -1 and VCAM-1 in mice aortic endothelial cells .Methods: The aor-tic endothelial cells in mice were cultivated , then MEF2A 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 MEF2A RNA interference group.MEF2A,ICAM-1, and VCAM-1 expressions were detected by ELISA , and mRNA levels of MEF2A,ICAM-1, and VCAM-1 were further examined by RT -PCR.Results: In the control group, NC group, and MEF2A 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 MEF2A RNA interference group was com-pared with the control group and NC group , there were significant differences (P <0.05).Conclusion: Lentivirus-mediated RNA interference of MEF2A could inhibit the expression of MEF2A and promote intravascular ICAM-1, VCAM-1 activity mRNA expression.

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