JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES)

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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

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

CLC Number: 

  • R373
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