title: PM2.5induced apoptosis in endothelial cell through the activation of the p53-bax-caspase pathway.
abstract: Exposure to airborne fine particulate matter (PM2.5) is associated with cardiovascular diseases (CVDs). Nevertheless, a comprehensive understanding of the underlying biological mechanisms by which PM2.5exposure 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 PM2.5in 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 PM2.5could significantly induce the apoptosis of HUVECs at the tested concentrations (0.2, 1, 5, 25 μg mL-1), compared with the negative control (p < 0.05, p < 0.01). The apoptotic rate of HUVECs increased with the elevating levels of PM2.5exposure, 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 PM2.5administration in the western blot, indicating that the intracellular approach of apoptosis, the p53-Bax-caspases pathway, is the major way of PM2.5-induced apoptosis in HUVECs. In conclusion, these results suggested that induction of EC apoptosis is an important mechanism by which ambient PM2.5exposure poses adverse effects on the cardiovascular system.
authors.affiliation: The School of Public Health, University of South China, Hengyang 421001, China; The Library, University of South China, Hengyang 421001, China.
authors.forename: Wuxiang
authors.initials: W
authors.lastname: Wang
authors.affiliation: The School of Public Health, University of South China, Hengyang 421001, China.
authors.forename: Ziyong
authors.initials: Z
authors.lastname: Deng
authors.affiliation: The College of Materials Science and Engineering, Jilin University, Changchun 130022, China.
authors.forename: Yuqin
authors.initials: Y
authors.lastname: Feng
authors.affiliation: The School of Public Health, University of South China, Hengyang 421001, China.
authors.forename: Fen
authors.initials: F
authors.lastname: Liao
authors.affiliation: The School of Public Health, University of South China, Hengyang 421001, China.
authors.forename: Furong
authors.initials: F
authors.lastname: Zhou
authors.affiliation: The School of Public Health, University of South China, Hengyang 421001, China. Electronic address: slfeng71@usc.edu.cn.
authors.forename: Shaolong
authors.initials: S
authors.lastname: Feng
authors.affiliation: The State Key Laboratory of Organic Geochemistry, Guangzhou Institute of Geochemistry, Chinese Academy of Sciences, Guangzhou 510640, China. Electronic address: wangxm@gig.ac.cn.
authors.forename: Xinming
authors.initials: X
authors.lastname: Wang
mesh_terms: D000393:Air Pollutants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D020169:Caspases / Q000378:metabolism; D002478:Cells, Cultured; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D052638:Particulate Matter / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
chemical_list: D000393:Air Pollutants; C494826:BAX protein, human; D052638:Particulate Matter; D019253:Proto-Oncogene Proteins c-bcl-2; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; D020169:Caspases
keywords: Apoptosis; Endothelial cell (EC); Fine particulate matter (PM(2.5)); Guangzhou; p53