Cigarette smoke extract induces aberrant @entity2247 methylation and apoptosis in XXXX umbilical vascular endothelial cells.

@entity1 @entity1977 @entity9736 @entity2823 @entity1030 @entity2247 @entity1981
UNASSIGNED: Cigarette smoke-induced apoptosis of vascular endothelial cells contributes to the pathogenesis of @entity1030 ( @entity1030 ). However, the mechanisms responsible for endothelial apoptosis remain poorly understood. We conducted an in vitro study to investigate whether DNA methylation is involved in smoking-induced endothelial apoptosis. @entity1 umbilical vascular endothelial cells (HUVECs) were exposed to @entity1981 ( @entity1981 ) at a range of concentrations (0 to 10%). HUVECs were also incubated with a demethylating reagent, 5-aza-2'-deoxycytidinem (AZA), with and without @entity1981 . Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated @entity1977 nick end labeling assay and flow cytometry using annexin V- @entity2823 /PI staining. We found that @entity1981 treatment significantly increased HUVEC apoptosis in a dose- and time-dependent manner. Quantitative real-time RT-PCR and immunoblot revealed that @entity1981 treatment decreased @entity2247 (COX II) mRNA and protein levels, and decreased COX activity. Methylation-specific PCR and direct @entity9736 sequencing revealed positive COX II gene methylation. AZA administration partly increased mRNA and protein expressions of COX II and COX activity decreased by @entity1981 , and attenuated the toxic effects of @entity1981 . Our results showed that @entity1981 induced aberrant COX II methylation and apoptosis in HUVECs.
