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目的:探讨细胞外信号调节激酶1/2(ERK1/2)信号通路在内皮微粒(EMPs)诱导人脐静脉内皮细胞(HU-VECs)表达细胞间黏附分子-1(ICAM-1)中的作用。方法:体外培养HUVECs,选取生长良好的第4～5代细胞,分为EMPs不同浓度作用组、EMPs不同时间作用组及ERKl/2特异性抑制剂组。应用蛋白免疫印迹法(Western blot)检测ICAM-1和磷酸化ERK1/2蛋白的表达。用实时荧光定量PCR(qRT-PCR)检测ICAM-1 mRNA的表达。结果:EMPs作用HUVECs后,ICAM-1 mRNA和其蛋白以及磷酸化ERK1/2蛋白的表达显著高于对照组,且呈浓度和时间依赖性的关系(均P<0.01);而ERKl/2特异性抑制剂PD98059对ICAM-1 mRNA和其蛋白以及磷酸化ERK1/2蛋白的表达,均有明显的抑制作用(均P<0.01)。结论:EMPs可诱导HUVECs中ICAM-1表达,其机制可能与激活ERK1/2信号通路有关。
AIM: To investigate the role of extracellular signal-regulated kinase 1/2 (ERK1 / 2) signaling pathway in the expression of intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HU-VECs) induced by endothelial progesterone . Methods: HUVECs were cultured in vitro. The cells of the 4th to 5th passage were selected and divided into different concentration groups of EMPs, different time groups of EMPs and specific ERK1 / 2 inhibitor group. The protein expressions of ICAM-1 and phosphorylated ERK1 / 2 were detected by Western blot. The expression of ICAM-1 mRNA was detected by real-time quantitative PCR (qRT-PCR). Results: After treated with EMPs, the expression of ICAM-1 mRNA and protein and phosphorylated ERK1 / 2 protein in HUVECs were significantly higher than those in control group (P <0.01), while ERK1 / 2 Inhibitory effect of PD98059 on ICAM-1 mRNA and its protein and phosphorylated ERK1 / 2 protein was significantly inhibited (all P <0.01). Conclusion: EMPs can induce the expression of ICAM-1 in HUVECs. The mechanism may be related to the activation of ERK1 / 2 signaling pathway.