Journal
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 23, Issue 10, Pages 10103-10113Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s11356-016-6253-9
Keywords
Air pollution; In vitro toxicology; Environmental toxicology; Fine particulate matter; MicroRNA; Apoptosis
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Funding
- National Natural Science Foundation of China [81472938]
- Fund of the Distinguished Talents of Jiangsu Province [BK20150021]
- Natural Science Foundation of Jiangsu Province [BK20151418]
- fund of the Distinguished Professor of Jiangsu Province
- Fundamental Research Funds for the Central Universities
- Science and Technology Support Project of Jiangsu Province [BE2011797]
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Studies have reported associations between fine particulate matter (PM2.5) and respiratory disorders; however, the underlying mechanism is not completely clear owing to the complex components of PM2.5. microRNAs (miRNAs) demonstrate tremendous regulation to target genes, which are sensitive to exogenous stimulation, and facilitate the integrative understood of biological responses. Here, significantly modulated miRNA were profiled by miRNA microarray, coupled with bioinformatic analysis; the potential biological function of modulated miRNA were predicted and subsequently validated by cell-based assays. Downregulation of miR-1228-5p (miR-1228(*)) expression in human A549 cells were associated with PM2.5-induced cellular apoptosis through a mitochondria-dependent pathway. Further, overexpression of miR-1228(*) rescued the cellular damages induced by PM2.5. Thus, our results demonstrate that PM2.5-induced A549 apoptosis is initiated by mitochondrial dysfunction and miR-1228(*) could protect A549 cells against apoptosis. The involved pathways and target genes might be used for future mechanistic studies.
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