@article {ZengP526, author = {Huihui Zeng and Ping Chen}, title = {Promoter methylation of Bcl-2 in CSE-induce HUVEC apoptosis}, volume = {42}, number = {Suppl 57}, elocation-id = {P526}, year = {2013}, publisher = {European Respiratory Society}, abstract = {Endothelia apoptosis participates copd and other diseases induced by smoking. We discussed whether Bcl-2 participated in cigarette smoke extract (CSE)-induce HUVEC apoptosis. Given the methylation in promoter causing gene silencing and existence of CpG islands in Bcl-2 promoter, we hypothesized that Bcl-2 methylation might induce the apoptosis.Method: HUVEC was treated with different CSE concentration. We divided and treated cells into four groups: control, 5\%CSE, 5\%CSE+AZA (demethylation reagent), and AZA. The apoptotic index, expression and methylation status of Bcl-2 were assessed through flowcytometry, westernblotting, and BSP respectively.Result: 1.CSE decreased Bcl-2 depend on concentation (Figure 1), and AZA prevented this abnormality.2.CSE increased methylation of Bcl-2 promoter (14.55{\textpm}3.15) \%, though AZA prevented the deregulation[(1.82{\textpm}1.57) \% P\<0.01].3.The regression analysis showed a relationship between Bcl-2 expression,apoptosis and methylation.Conclusion: CSE induced abnormal methylation of Bcl-2 promoter, which might participate endothelia apoptosis. This high methylation of Bcl-2 promoter might be involved in COPD and other endothelia relative diseases.}, issn = {0903-1936}, URL = {https://erj.ersjournals.com/content/42/Suppl_57/P526}, eprint = {https://erj.ersjournals.com/content/42/Suppl_57/P526.full.pdf}, journal = {European Respiratory Journal} }