title: p53-Dependent apoptosis induced in human bronchial epithelial (16-HBE) cells by PM(2.5) sampled from air in Guangzhou, China.
abstract: Epidemiological studies have shown that air pollution particulate matter (PM) is associated with increased respiratory morbidity and mortality. However, the mechanisms are not fully understood. Oxidative stress-mediated apoptosis plays an important role in the occurrence of respiratory diseases. In this study, human bronchial epithelial (16-HBE) cells were exposed to different concentrations (16-128 µg/ml) of PM(2.5) for 24 h to investigate the apoptosis induced by PM(2.5). The results showed that PM(2.5) exposure significantly induced apoptosis, DNA strand breaks, and oxidative damage in a dose-dependent manner in 16-HBE cells. The expression of p53 and p73 increased significantly along with the dose of PM(2.5) in 16-HBE cells, whereas the expression of p21(Cip1/WAF1) decreased; the expression of mdm2 increased and then decreased, but not significantly. Taken together, these observations indicate that PM(2.5) may lead to oxidative damage and induce apoptosis through the p53-dependent pathway in 16-HBE cells. p53-Dependent apoptosis mediated by DNA strand breaks may be an important mechanism of PM(2.5)-induced apoptosis in 16-HBE cells.
authors.affiliation: School of Public Health, Guangxi Medical University , Nanning, Guangxi , China .
authors.forename: Bo
authors.initials: B
authors.lastname: Zhou
authors.forename: Guiqiang
authors.initials: G
authors.lastname: Liang
authors.forename: Huiyan
authors.initials: H
authors.lastname: Qin
authors.forename: Xiaowu
authors.initials: X
authors.lastname: Peng
authors.forename: Jiongli
authors.initials: J
authors.lastname: Huang
authors.forename: Qin
authors.initials: Q
authors.lastname: Li
authors.forename: Li
authors.initials: L
authors.lastname: Qing
authors.forename: Li'e
authors.initials: L
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Chen
authors.forename: Li
authors.initials: L
authors.lastname: Ye
authors.forename: Piye
authors.initials: P
authors.lastname: Niu
authors.forename: Yunfeng
authors.initials: Y
authors.lastname: Zou
mesh_terms: D000397:Air Pollution / Q000009:adverse effects*; D017209:Apoptosis / Q000187:drug effects*; D001980:Bronchi / Q000187:drug effects* / Q000378:metabolism; D002460:Cell Line; D002681:China; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D053960:DNA Breaks; D004268:DNA-Binding Proteins / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D004784:Environmental Monitoring; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007700:Kinetics; D009687:Nuclear Proteins / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D009994:Osmolar Concentration; D018384:Oxidative Stress / Q000187:drug effects; D052638:Particulate Matter / Q000633:toxicity*; D051736:Proto-Oncogene Proteins c-mdm2 / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D012111:Residence Characteristics; D020545:Respiratory Mucosa / Q000187:drug effects* / Q000378:metabolism; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53 / Q000819:agonists* / Q000235:genetics / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D014504:Urban Health
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D052638:Particulate Matter; C495901:TP53 protein, human; C000606460:TP73 protein, human; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; C497206:MDM2 protein, human; D051736:Proto-Oncogene Proteins c-mdm2
keywords: Apoptosis; DNA damage; PM2.5; oxidative stress; p53