PM2.5 induced apoptosis in endothelial cell through the activation of the p53-bax-caspase pathway.

Abstract Exposure to airborne fine particulate matter (PM 2.5 ) is associated with cardiovascular diseases (CVDs). Nevertheless, a comprehensive understanding of the underlying biological mechanisms by which PM 2.5 exposure induces or aggravates CVDs remain insufficiently clear. In the present study, the flow cytometry was employed to investigate the apoptosis of human umbilical vein endothelial cells (HUVECs) induced by PM 2.5 in culture. The underlying apoptotic pathway was also studied through the determination of the protein expression and activation of p53, Bax, Bcl-2, caspases-9, -7, -3, and PARP by western blot. The results showed that PM 2.5 could significantly induce the apoptosis of HUVECs at the tested concentrations (0.2, 1, 5, 25 μg mL −1 ), compared with the negative control (p  2.5 exposure, showing a clear dose-effect relationship. Moreover, the increasing phosphorylation of p53, decreasing ratio of Bcl-2/Bax, and enhancing activation of the downstream proteins caspase-9, -7, -3 and PARP, were also observed with the increasing concentrations of PM 2.5 administration in the western blot, indicating that the intracellular approach of apoptosis, the p53-Bax-caspases pathway, is the major way of PM 2.5 -induced apoptosis in HUVECs. In conclusion, these results suggested that induction of EC apoptosis is an important mechanism by which ambient PM 2.5 exposure poses adverse effects on the cardiovascular system.