p53-Dependent apoptosis induced in human bronchial epithelial (16-HBE) cells by PM(2.5) sampled from air in Guangzhou, China

Toxicol Mech Methods. 2014 Dec;24(8):552-9. doi: 10.3109/15376516.2014.951814.

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.

Keywords: Apoptosis; DNA damage; PM2.5; oxidative stress; p53.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Air Pollution / adverse effects*
  • Apoptosis / drug effects*
  • Bronchi / drug effects*
  • Bronchi / metabolism
  • Cell Line
  • China
  • Cyclin-Dependent Kinase Inhibitor p21 / antagonists & inhibitors
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • DNA Breaks
  • DNA-Binding Proteins / agonists
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Environmental Monitoring
  • Gene Expression Regulation / drug effects
  • Humans
  • Kinetics
  • Nuclear Proteins / agonists
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Osmolar Concentration
  • Oxidative Stress / drug effects
  • Particulate Matter / toxicity*
  • Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors
  • Proto-Oncogene Proteins c-mdm2 / chemistry
  • Proto-Oncogene Proteins c-mdm2 / genetics
  • Proto-Oncogene Proteins c-mdm2 / metabolism
  • Residence Characteristics
  • Respiratory Mucosa / drug effects*
  • Respiratory Mucosa / metabolism
  • Tumor Protein p73
  • Tumor Suppressor Protein p53 / agonists*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Proteins / agonists
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism
  • Urban Health*

Substances

  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • DNA-Binding Proteins
  • Nuclear Proteins
  • Particulate Matter
  • TP53 protein, human
  • TP73 protein, human
  • Tumor Protein p73
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2