摘要
目的:研究HIV-1Nef基因对内皮细胞ECV304细胞ICAM-1表达的影响及其信号途径。方法:选用Nef基因稳定表达细胞株ECV304-Nef和对照细胞株ECV304pcDNA3.1(+),应用Westernblot分析ECV304-Nef细胞ERK的磷酸化水平,利用ERK磷酸化抑制剂通过Westernblot、流式细胞术分析ECV304-Nef细胞ICAM-1的表达水平与信号分子ERK磷酸化的相关性。结果:Westernblot显示ECV304-Nef细胞ICAM-1和p-ERK蛋白的表达水平均高于对照组;流式细胞术检测结果表明ECV304-Nef细胞和对照组ICAM-1阳性细胞百分率分别为(35.3±2.2)%和(12.5±0.8)%(P<0.01)。加入p-ERK抑制剂PD98059后,ECV304-Nef细胞p-ERK水平被显著抑制,ICAM-1降至对照组水平,ECV304-Nef细胞和对照组细胞ICAM-1阳性细胞百分率分别为(11.4±1.1)%和(10.4±1.5)%(P>0.05)。结论:HIV-1Nef基因上调血管内皮细胞细胞黏附分子ICAM-1的表达与ERK信号分子磷酸化有关,为HIV-1感染的致病机制及临床治疗提供实验基础。
AIM：To explore the effect of HIV-1 Nef on the ICAM-1 expression of endothelial cells ECV-304 and its signaling pathways.METHODS：ICAM-1 expression on the endothelial cells ECV-304 was detected by Western blot and FCM assay.Kinase inhibitor PD98059 was used in the cells to analyze the ERK signaling pathway.RESULTS：Western blot showed that ICAM-1 and p-ERK protein expression increased in Nef expressed ECV304 cells（ECV304-Nef）and FCM results showed that the percentage of ICAM-1 positive cells in ECV304-Nef and control cells was（35.3±2.2）% and（12.5±0.8）% respectively（P〈0.01）.p-ERK inhibitor PD98059 almost completely blocked the Nef up-regulation of the p-ERK and ICAM-1.When p-ERK inhibitor was added,the percentage of ICAM-1 positive cells in ECV304-Nef（11.4±1.1）% was reduced to the level of the control cells（10.4±1.5）%（P〉0.05）.CONCLUSION：Erk/Mapk signaling pathway may contribute to the over-expression of adhesion molecules ICAM-1 gene in HIV-1 Nef positive cells.These findings may provide the basis for further research on the mechanism and treatment of HIV-1 infection.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2010年第1期44-46,共3页
Chinese Journal of Cellular and Molecular Immunology
基金
宜昌市科技发展计划项目(A2007108-02b02)
三峡大学留学回国人才基金项目资助(2007)
