Abstract：
:Crotonaldehyde is an environment pollutant and lipid peroxidation product. Crotonaldehyde produces adverse effects to humans and serves as a risk factor for human pulmonary diseases. Like acrolein and 4-hydroxynonenal, crotonaldehyde seems likely to alter many cell signaling cascades, including inflammatory responses. The purpose of this study was to investigate the genome-wide transcriptional responses of normal human bronchial epithelial cells exposed to crotonaldehyde. Using microarrays technology, the global changes in transcriptional level were analyzed. Prior to RNA extraction, cells were exposed to crotonaldehyde at 40 or 80 microM for 3 or 6h. Real-time quantitative polymerase chain reaction (qPCR) was performed to validate microarray data and cell cycle arrest was determined. The commonly differentially regulated genes in many biological processes were dysregulated including inflammatory responses, exogenous metabolism, cell cycle, heat shock responses, and antioxidant responses. Results in the present study screen out the important roles of HMOX1 in regulating other signaling cascades and ALDH1A3 in detoxifying exogenous toxicants. Collectively, our study demonstrated that crotonaldehyde altered gene expression profile in the genome-wide transcriptional level in normal human bronchial epithelial cells. And many of them represented potential mechanisms of crotonaldehyde causing cytotoxicity and tissue injury in the human lung.
journal_name
Toxicol Lettjournal_title
Toxicology lettersauthors
Liu XY,Yang ZH,Pan XJ,Zhu MX,Xie JPdoi
10.1016/j.toxlet.2010.05.005subject
Has Abstractpub_date
2010-08-16 00:00:00pages
113-22issue
2eissn
0378-4274issn
1879-3169pii
S0378-4274(10)01506-7journal_volume
197pub_type
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