Differential Expressed Genes in ECV304 Endothelial-Like Cells Infected with Herpes Simplex Virus Type 2

Herpes simplex virus (HSV), the viral agent causing human genital herpes, recurs easily and poses significant harm to patients, while also being associated with atherosclerosis (AS). Currently, no effective therapy or vaccine exists to combat HSV. Previous studies have demonstrated the presence of HSV and its DNA in AS-diseased tissue, yet the precise pathogenesis of HSV involvement remains unclear. To investigate the genetic mechanism of HSV-induced vascular endothelial injury and AS, a type of human umbilical vein endothelial cells (ECV-304 cells) cultured in vitro were infected with herpes simplex virus type 2 (HSV-2). The effect of HSV-2 on differential gene expression in ECV304 cells was investigated by gene microarray technology during the early stages of infection. The results revealed a total of 462 differentially expressed genes, with 318 genes exhibiting up-regulated expression and 144 genes showing down-regulated expression. Furthermore, bioinformatics analysis revealed that all 462 differentially expressed genes were implicated in 237 distinct biological processes. Notably, 79 of these biological processes demonstrated statistically significant differences (P < 0.05), encompassing critical functions such as protein synthesis, ribosome biogenesis and assembly, as well as DNA and mRNA metabolism. Our findings have unveiled the differentially expressed genes of HSV-2 in ECV304 cells during infection, offering crucial insights into the pathogenic mechanisms underlying HSV-2 invasion of endothelial cells and the pathobiology of AS.

Effect of polysaccharide sulfate 916 on the production of nitric oxide in ECV3 04 cells induced by cytokines and H_2O_2

To investigate the effect of polysaccharide sulfate 916 (PS916) on the productio n of nitric oxide (NO) in ECV304 cells induced by tumor necrosis factor α (TNF α), interleukin 1β (IL 1β) and H 2O 2 in vitro Methods Production of NO in ECV304 cells was measured by the Griess method and the proli feration of cells was tested by the MTT method The activity of NO synthase was detected spectrophotometrically Results Production of NO in ECV304 cells decreased after treatment with 40?ng/ml IL 1 β and 40?ng/ml TNFα, but increased in the presence of H 2O 2 0 1?mmol/L PS916 significantly enhanced NO production in ECV304 cells in a dose depende nt manner in the TNFα and IL 1β treated groups and decreased it in the H 2O 2 treated group Proliferation of ECV304 cells was inhibited by TNFα and H 2O 2 and no effect was found in the IL 1β treated group PS916 increased the proliferation of cells treated with TNFα and H 2O 2 dose dependently In vitro, PS916 has no effect on the activity of NO synthase Conclusion PS916 has a protective effect on ECV304 cells exposed to IL 1β, TNFα and H 2 O 2

Effect of polysaccharide sulfate 916 on the production of nitric oxide in ECV3 04 cells induced by cytokines and H2O2

To investigate the effect of polysaccharide sulfate 916 (PS916) on the productio n of nitric oxide (NO) in ECV304 cells induced by tumor necrosis factor α (TNF α), interleukin 1β (IL 1β) and H 2O 2 in vitro Methods Production of NO in ECV304 cells was measured by the Griess method and the proli feration of cells was tested by the MTT method The activity of NO synthase was detected spectrophotometrically Results Production of NO in ECV304 cells decreased after treatment with 40?ng/ml IL 1 β and 40?ng/ml TNFα, but increased in the presence of H 2O 2 0 1?mmol/L PS916 significantly enhanced NO production in ECV304 cells in a dose depende nt manner in the TNFα and IL 1β treated groups and decreased it in the H 2O 2 treated group Proliferation of ECV304 cells was inhibited by TNFα and H 2O 2 and no effect was found in the IL 1β treated group PS916 increased the proliferation of cells treated with TNFα and H 2O 2 dose dependently In vitro, PS916 has no effect on the activity of NO synthase Conclusion PS916 has a protective effect on ECV304 cells exposed to IL 1β, TNFα and H 2 O 2