Journal
SCIENTIFIC REPORTS
Volume 2, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep00275
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Funding
- National Institute of Health [ES015024, ES013995, HL071643, HL092963, T32HL076139]
- Northwestern University Clinical and Translational Sciences Institute (NUCATS) Center for Translational Innovation (CTI) from the National Center for Research Resources (NCCR) [UL1 RR025741]
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Exposure of human populations to chronically elevated levels of ambient particulate matter air pollution <2.5 mu m in diameter (PM2.5) has been associated with an increase in lung cancer incidence. Over 70% of lung cancer cell lines exhibit promoter methylation of the tumor suppressor p16, an epigenetic modification that reduces its expression. We exposed mice to concentrated ambient PM2.5 via inhalation, 8 hours daily for 3 weeks and exposed primary murine alveolar epithelial cells to daily doses of fine urban PM (5 mu g/cm(2)). In both mice and alveolar epithelial cells, PM exposure increased ROS production, expression of the DNA methyltransferase 1 (DNMT1), and methylation of the p16 promoter. In alveolar epithelial cells, increased transcription of DNMT1 and methylation of the p16 promoter were inhibited by a mitochondrially targeted antioxidant and a JNK inhibitor. These findings provide a potential mechanism by which PM exposure increases the risk of lung cancer.
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