[人类免疫缺陷病毒1型负调控因子通过细胞外信号调节激酶/丝裂原活化蛋白激酶信号通路调控内皮细胞上细胞间黏附分子-1的表达]
[HIV-1 Nef regulates ICAM-1 expression on endothelial cells via Erk /Mapk signaling pathway].
作者信息
Yang Fan, Liu Chao-qi, Qin Xiao-lin, Shi Ji-jing
机构信息
Department of Internal Medicine, Second People's Hospital of Yichang, Yichang 443000, China.
出版信息
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2010 Jan;26(1):44-6.
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.
目的
探讨HIV-1 Nef对内皮细胞ECV-304细胞间黏附分子-1（ICAM-1）表达及其信号通路的影响。
方法
采用蛋白质免疫印迹法（Western blot）和流式细胞术（FCM）检测ECV-304细胞中ICAM-1的表达。用激酶抑制剂PD98059作用于细胞，分析细胞外信号调节激酶（ERK）信号通路。
结果
蛋白质免疫印迹法显示，表达Nef的ECV304细胞（ECV304-Nef）中ICAM-1和磷酸化ERK（p-ERK）蛋白表达增加；流式细胞术结果显示，ECV304-Nef细胞和对照细胞中ICAM-1阳性细胞百分比分别为（35.3±2.2）%和（12.5±0.8）%（P>0.01）。p-ERK抑制剂PD98059几乎完全阻断了Nef对p-ERK和ICAM-1的上调作用。加入p-ERK抑制剂后，ECV304-Nef细胞中ICAM-1阳性细胞百分比由（11.4±1.1）%降至对照细胞水平（10.4±1.5）%（P>0.05）。
结论
Erk/丝裂原活化蛋白激酶（Mapk）信号通路可能参与HIV-1 Nef阳性细胞中黏附分子ICAM-1基因的过表达。这些研究结果可能为进一步研究HIV-1感染的机制和治疗提供依据。
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