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山东大学学报(医学版)

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人巨细胞病毒感染致血管内皮细胞损伤机制的研究

王凤,吴建敏,周亚滨,李树英,程轶喆,齐眉,唐伟,王红,刘娟,于晗   

  1. 实验畸形学教育部重点实验室山东大学医学院微生物学教研室, 济南 250012
  • 收稿日期:2007-08-02 修回日期:1900-01-01 出版日期:2007-11-24 发布日期:2007-11-24
  • 通讯作者: 周亚滨

Mechanisms of vascular endothelial cell injury induced by human cytomegalovirus

WANG Feng, WU Jian-min, ZHOU Ya-bin, LI Shu-ying, CHENG Yi-zhe, QI Mei, TANG Wei, WANG Hong, LIU Juan, YU Han   

  1. Key Laboratory of Experimental Teratology, Ministry of Education, China; Department of Microbiology, School of Medicine, Shandong University, Jinan 250012, China
  • Received:2007-08-02 Revised:1900-01-01 Online:2007-11-24 Published:2007-11-24
  • Contact: ZHOU Ya-bin

摘要: 摘要:目的观察人巨细胞病毒(HCMV)感染对人血管内皮细胞氧化应激的影响及对血管细胞粘附分子-1(VCAM-1)和糖基化终产物受体(RAGE)时序性表达的影响,研究HCMV感染致动脉粥样硬化(AS)的作用机制。方法用HCMV感染血管内皮细胞,用激光共聚焦显微镜检测细胞内活性氧(ROS)的改变;采用RT-PCR方法检测不同感染时段细胞VCAM-1及RAGEmRNA的表达。结果HCMV感染血管内皮细胞后,HCMV组荧光强度显著高于对照组(P<0.01)。感染0h时,VCAM-1mRNA有基础水平的表达,4h开始升高,8h时达高峰,12h开始回落,24h回落更明显,与0h比较,均有统计学意义(P<0.01),48h接近0h表达水平(P>0.05)。感染0h时,RAGEmRNA有基础水平的表达,4h开始升高,8h时表达水平明显升高,随感染时间延长,表达量逐渐增高,感染24h时达高峰,48h开始回落,仍维持在较高的水平,各时段与0h比较,均有统计学意义(P<0.01)。结论HCMV感染血管内皮细胞后能够增强氧化应激,促进VCAM-1及RAGE的mRNA表达,并且呈时间依赖性。HCMV有可能通过增强氧化应激、上调VCAM-1及RAGE的表达介导血管内皮细胞的炎症反应,促进动脉粥样硬化的发生、发展。

关键词: 糖基化终产物, 受体 , 活性氧, 血管细胞粘附分子-1, 脐静脉, 巨细胞病毒

Abstract: ObjectiveTo explore the mechanisms of cytomegalovirus infection by investigating the changes of reactive oxygen species (ROS) and sequential changes of the vascular cell adhesion molecule-1 (VCAM-1) and the receptors for advanced glycation end products (RAGE) in vascular endothelial cells with human cytomegalovirus(HCMV) infection. MethodsVascular endothelial cells were cultured and then infected by HCMV, then changes of reactive oxygen species were identified by confocal microscopy. Expressions of VCAM-1 and RAGE mRNA were determined by reverse transcriptase polymerase chain reaction. ResultsFluorescence intensity was determined at a low level in the control group and was significantly increased in the HCMV group (P<0.01). VCAM-1 mRNA was expressed at a low level at 0 hour, began to increase at 4 hours after HCMV infection and reached a peak at 8 hours. After 12 hours, it began to decrease and significantly decreased at 24 hours, but it was higher than that at 0 hour (P<0.01). At 48 hours, the VCAM-1 mRNA level was close to that at 0 hour (P>0.05). RAGE mRNA was expressed at a low level in the control group, began to increase 4 hours after HCMV infection, increased to a significant level at 12 hours, and reached a peak at 24 hours. It significantly decreased but remained at a relatively high level at 48 hours (P<0.01). ConclusionsHCMV infection can enhance the oxidative stress and the expressions of VCAM-1 and RAGE mRNA in vascular endothelial cells and it may induce an inflammatory reaction by enhancing the oxidative stress and up-regulating the VCAM-1 and RAGE expressions in endothelial cells, which further facilitates the occurrence and development of atherosclerosis.

Key words: Cytomegalovirus, Umbilical veins, Reactive oxygen species, Vascular cell adhesion molecule-1, Advanced glycation end products, Receptor

中图分类号: 

  • R373
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