Regulation of human lung epithelial cell numbers by diesel exhaust particles

Bayram, H; Ito, K; Issa, R; Ito, M; Sukkar, M; Chung, KF

Regulation of human lung epithelial cell numbers by diesel exhaust particles

Bayram, H Ito, K Issa, R Ito, M Sukkar, M

Chung, KF

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Publication Type:: Journal Article
Citation:: European Respiratory Journal, 2006, 27 (4), pp. 705 - 713
Issue Date:: 2006-04-01

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Field	Value	Language
dc.contributor.author	Bayram, H	en_US
dc.contributor.author	Ito, K	en_US
dc.contributor.author	Issa, R	en_US
dc.contributor.author	Ito, M	en_US
dc.contributor.author	Sukkar, M https://orcid.org/0000-0003-4591-2399	en_US
dc.contributor.author	Chung, KF	en_US
dc.date.issued	2006-04-01	en_US
dc.identifier.citation	European Respiratory Journal, 2006, 27 (4), pp. 705 - 713	en_US
dc.identifier.issn	0903-1936	en_US
dc.identifier.uri	http://hdl.handle.net/10453/26808
dc.description.abstract	Particulate air pollution is associated with respiratory morbidity and has cytotoxic and proinflammatory effects. The effects of diesel exhaust particles (DEP) on proliferation and apoptosis of A549 lung epithelial cells were examined. When deprived of serum (serum starvation), epithelial cell numbers fell, but DEP (5-200 μg·mL-1) prevented this. Using flow cytometric analysis of propidium iodide (PI) staining, DEP (10 μg·mL-1) increased cells in the S phase of cell cycle from 12.85 to 18.75% after 48 h, reversing serum starvation-induced G0/1 arrest. DEP also reduced the increase in apoptotic cells, as defined by double expression of annexin V/PI, observed after serum starvation (from 28.35 to 15.46%). The antioxidants, N-acetylcysteine (NAC; 33 mM) and AEOL10113 (10-100 μM), the N-terminal c-jun kinase inhibitor, SP600125 (33 μM), and nuclear factor-κB inhibitor, SN50 (33 μM), inhibited DEP-induced cell number increase. NAC inhibited DEP-induced reduction of G0/1 and increase in cells in the S and G2/M phases. Expression of p21CIP1/WAF1 mRNA and protein seen with serum starvation was reduced by DEP. In conclusion, diesel exhaust particles prevented serum starvation-led decreases in A549 epithelial cells by inducing cell cycle progression and preventing apoptosis, processes involving oxidative stress, inhibition of p21CIP1/WAF1 expression and stimulation of N-terminal c-jun kinase and nuclear factor-κB. Therefore, low-dose diesel exhaust particle exposure may lead to lung epithelial cell hyperplasia. Copyright © ERS Journals Ltd 2006.	en_US
dc.relation.ispartof	European Respiratory Journal	en_US
dc.relation.isbasedon	10.1183/09031936.06.00012805	en_US
dc.subject.classification	Respiratory System	en_US
dc.subject.mesh	Respiratory Mucosa	en_US
dc.subject.mesh	Epithelial Cells	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Pneumonia	en_US
dc.subject.mesh	Cyclin E	en_US
dc.subject.mesh	NF-kappa B	en_US
dc.subject.mesh	RNA, Messenger	en_US
dc.subject.mesh	Cell Count	en_US
dc.subject.mesh	Vehicle Emissions	en_US
dc.subject.mesh	Cell Cycle	en_US
dc.subject.mesh	Cell Division	en_US
dc.subject.mesh	Apoptosis	en_US
dc.subject.mesh	Gene Expression	en_US
dc.subject.mesh	Oxidative Stress	en_US
dc.subject.mesh	Particle Size	en_US
dc.subject.mesh	Cyclin-Dependent Kinase Inhibitor p21	en_US
dc.subject.mesh	Cyclin-Dependent Kinase 2	en_US
dc.title	Regulation of human lung epithelial cell numbers by diesel exhaust particles	en_US
dc.type	Journal Article
utslib.citation.volume	4	en_US
utslib.citation.volume	27	en_US
utslib.for	110203 Respiratory Diseases	en_US
utslib.for	1116 Medical Physiology	en_US
utslib.for	11 Medical and Health Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Graduate School of Health
utslib.copyright.status	closed_access
pubs.issue	4	en_US
pubs.publication-status	Published	en_US
pubs.volume	27	en_US

Abstract:

Particulate air pollution is associated with respiratory morbidity and has cytotoxic and proinflammatory effects. The effects of diesel exhaust particles (DEP) on proliferation and apoptosis of A549 lung epithelial cells were examined. When deprived of serum (serum starvation), epithelial cell numbers fell, but DEP (5-200 μg·mL-1) prevented this. Using flow cytometric analysis of propidium iodide (PI) staining, DEP (10 μg·mL-1) increased cells in the S phase of cell cycle from 12.85 to 18.75% after 48 h, reversing serum starvation-induced G0/1 arrest. DEP also reduced the increase in apoptotic cells, as defined by double expression of annexin V/PI, observed after serum starvation (from 28.35 to 15.46%). The antioxidants, N-acetylcysteine (NAC; 33 mM) and AEOL10113 (10-100 μM), the N-terminal c-jun kinase inhibitor, SP600125 (33 μM), and nuclear factor-κB inhibitor, SN50 (33 μM), inhibited DEP-induced cell number increase. NAC inhibited DEP-induced reduction of G0/1 and increase in cells in the S and G2/M phases. Expression of p21CIP1/WAF1 mRNA and protein seen with serum starvation was reduced by DEP. In conclusion, diesel exhaust particles prevented serum starvation-led decreases in A549 epithelial cells by inducing cell cycle progression and preventing apoptosis, processes involving oxidative stress, inhibition of p21CIP1/WAF1 expression and stimulation of N-terminal c-jun kinase and nuclear factor-κB. Therefore, low-dose diesel exhaust particle exposure may lead to lung epithelial cell hyperplasia. Copyright © ERS Journals Ltd 2006.

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http://hdl.handle.net/10453/26808