Herpes simplex virus 1 induced LOX-1 expression in an endothelial cell line, ECV 304.
Infections, such as by Chlamydophilia pneumoniae, cytomegalovirus, herpes simplex virus, and Helicobacter pylori, have been shown to be involved in atherogenesis. Herpes simplex virus I (HSV-1) could infect vascular endothelial cells, and it has been shown that, when endothelial cells were activated with oxidized LDL (oxLDL), a number of cellular events are occurred, leading to endothelial cell dysfunction. Since LOX-1 is a major receptor for oxLDL on endothelial cells and its expression was increased in atherosclerosis, we investigated whether HSV1 infection can lead to the increase expression of LOX-1 in endothelial cells. LOX-1 mRNA expression determined by RT-PCR and LOX-1 promoter activity measured by luciferase assay were increased in endothelial cells following HSV-1 infection. This suggests that one of the mechanisms by which HSV-1 is involved in atherogenesis maybe the enhanced uptake of oxLDL via the increased expression of LOX-1 in endothelial cells.
Department of Microbiology, Chulalongkorn University, Bangkok, Thailand. fmedcch@md.chula.ac.th
C
C
Chirathaworn
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Pongpanich
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Poovorawan
D001161:Arteriosclerosis / Q000378:metabolism; D002460:Cell Line; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000821:virology*; D018259:Herpesvirus 1, Human / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D011973:Receptors, LDL / Q000235:genetics / Q000378:metabolism*; D051131:Receptors, Oxidized LDL
D008077:Lipoproteins, LDL; D012333:RNA, Messenger; D011973:Receptors, LDL; D051131:Receptors, Oxidized LDL