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

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WOS被引频次:6
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成果类型:
期刊论文
作者:
Wang, Wuxiang;Deng, Ziyong;Feng, Yuqin;Liao, Fen;Zhou, Furong;Feng, Shaolong;Wang, Xinming
通讯作者:
Feng, Shaolong(slfeng71@usc.edu.cn)
作者机构:
[ Feng, Shaolong ; Liao, Fen ; Deng, Ziyong ; Wang, Wuxiang ; Zhou, Furong ] The School of Public Health, University of South China, Hengyang, 421001, China
[ Feng, Yuqin ] The College of Materials Science and Engineering, Jilin University, Changchun, 130022, China
[Wang, Wuxiang ] The Library, University of South China, Hengyang, 421001, China
[ Wang, Xinming ] The State Key Laboratory of Organic Geochemistry, Guangzhou Institute of Geochemistry, Chinese Academy of Sciences, Guangzhou, 510640, China
通讯机构:
[Feng, Shaolong] The School of Public Health, University of South China, Hengyang 421001, China. Electronic address:
[Wang, Xinming] The State Key Laboratory of Organic Geochemistry, Guangzhou Institute of Geochemistry, Chinese Academy of Sciences, Guangzhou 510640, China. Electronic address:
语种:
英文
关键词:
Apoptotic pathways - Biological mechanisms - Cardio-vascular disease - Dose-effect relationships - Fine particulate matter - Guangzhou - Human umbilical vein endothelial cells - Protein expressions
期刊:
Chemosphere
年:
2017
卷:
177
页码:
135-143
文献类别:
WOS:Article;EI:Journal article (JA)
所属学科:
ESI学科类别:环境科学/生态学;WOS学科类别:Environmental Sciences
入藏号:
PMID:28284960
基金类别:
Natural Science Foundation of China [41571130031, 41530641]; Hunan Province [2016JJ2113]; Foundation of Educational Department of Hunan Province [12A118]; University of South China, China [2012XQD44]
机构署名:
本校为第一且通讯机构
院系归属:
公共卫生学院
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摘要:
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 PM2.5 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 PM2.5 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 PM2.5 could significantly induce the apoptosis of HUVECs at the tested concentrations (0.2, 1, 5, 25 mug mL-1), compared with the negative control (p < 0.05, p < 0.01). The apoptotic rate of HUVECs increased with the elevating levels of PM2.5 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 PM2.5 administration 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 PM2.5 exposure poses adverse effects on the cardiovascular system.
参考文献:
Bonetti PO, 2003, ARTERIOSCL THROM VAS, V23, P168, DOI 10.1161/01.ATV.0000051384.43104.FC
Brook RD, 2010, CIRCULATION, V121, P2331, DOI 10.1161/CIR.0b013e3181dbece1
Collaborators GRF, 2015, LANCET, V386, P2287
Danial NN, 2004, CELL, V116, P205, DOI 10.1016/S0092-8674(04)00046-7
Davignon J, 2004, CIRCULATION, V109, P27, DOI 10.1016/01.CIR.0000131515.03336.f8

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