title: Herpes simplex virus 2 infects human endothelial ECV304 cells and induces cell apoptosis synergistically with ox-LDL.
abstract: Virus infection has been shown to accelerate atherosclerosis. Serological studies indicate a link between the Herpes simplex virus (HSV) infection and atherosclerosis, which is initiated and progression of which is promoted by such factors as oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction. In order to recognize the direct role of HSV-2 in endothelial dysfunction, the present study investigated the infection of HSV-2 in endothelial ECV304 cells and the induction of cell apoptosis in the presence of ox-LDL. We firstly examined the HSV-2 infection by immunohistochemical assay for viral gB protein, quantitative PCR for viral ICP4 mRNA, or via virus growth determination. Then we investigated the regulation of HSV-2 infection on the cell viability and apoptosis, in the absence or presence of ox-LDL. In addition, we analyzed the apoptosis-associated molecules in the HSV-2-infected ECV304 cells. The results demonstrated that HSV-2 infected endothelial ECV304 cells and replicated efficiently, and the virus infection significantly reduced the cell viability and significantly induced cell apoptosis; particularly, cell viability reduction and cell apoptosis induction were aggravated by the ox-LDL presence. Moreover, the western blot assay confirmed the apoptosis induction; there was a significantly high level of released cytochrome c, activated caspase 3 and lyzed Poly (ADP-ribose) polymerase (PARP) by the activated caspase 3 in the HSV-2-infected ECV304 cells, particularly the cells subject to ox-LDL. Thus, we confirmed that HSV-2 infected endothelial ECV304 cells, induced cell apoptosis, which was aggravated by ox-LDL.
authors.affiliation: Health wards, The Affiliated Hospital of Inner Mongolia Medical University.
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Zhang
authors.forename: Qizhu
authors.initials: Q
authors.lastname: Tang
authors.forename: Li
authors.initials: L
authors.lastname: Xu
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D050197:Atherosclerosis / Q000209:etiology; D053148:Caspase 3 / Q000378:metabolism; D002478:Cells, Cultured; D045304:Cytochromes c / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects* / Q000201:enzymology / Q000821:virology*; D018258:Herpesvirus 2, Human / Q000472:pathogenicity*; D006801:Humans; D008077:Lipoproteins, LDL / Q000009:adverse effects*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism
chemical_list: D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D045304:Cytochromes c; D011065:Poly(ADP-ribose) Polymerases; D053148:Caspase 3