Inhibiting DNA methylation alleviates cigarette smoke extract-induced dysregulation of Bcl-2 and endothelial apoptosis.

ABSTRACT:

Introduction

There is evidence that cigarette smoking participates in disease progression through endothelial apoptosis. Bcl-2 family proteins are essential and critical regulators of apoptosis. We explored whether Bcl-2 plays a role in cigarette smoke extract induced (CSE-induced) endothelial apoptosis. Furthermore, given the involvement of epigenetics in apoptosis and Bcl-2 expression, we hypothesized that CSE-induced apoptosis might be caused by gene methylation.

Methods

Human umbilical vascular endothelial cells (HUVECs) were treated with CSE, CSE plus 5-aza-2'-deoxycytidine (AZA, an inhibitor of DNA methylation), or AZA and phosphate-buffered saline (PBS). Endothelial apoptosis was determined by Annexin-V and propidium iodide staining. The expression levels of Bcl-2, Ba

SUBMITTER: Zeng H 

PROVIDER: S-EPMC7291961 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature