Transcriptomic analyses of human bronchial epithelial cells BEAS-2B exposed to atmospheric fine particulate matter PM2.5

- The changes of gene expression profile induced by PM2.5 were investigated.
- BEAS-2B cells were treated with 15.625 μg/cm2 of PM2.5 for 24 h.
- Microarray analysis and bioinformatics analysis were introduced.
- Genes associated with antioxidant and inflammatory response were up-regulated.
- Genes related to cell proliferation and mitosis regulation were down-regulated.

Respiratory exposure is the major route of atmospheric PM2.5 entering the human body. Epidemiological studies have indicated that exposure to PM2.5 is associated with increased risk of pulmonary diseases, but the underlying mechanisms remain less clear. In this study, human bronchial epithelial cells (BEAS-2B) were used to investigate the toxic effect and gene expression changes induced by PM2.5 collected from Beijing, China, based on microarray and following bioinformatic analyses. Gene ontology (GO) analysis indicated that PM2.5 caused significant changes in gene expression patterns related to a series of important functions, covering gene transcription, signal transduction, cell proliferation, cellular metabolic processes, immune response, etc. Additionally, pathway analysis and signal-net analysis showed that PI3K/Akt, MAPK, and TNF signaling pathways were the most prominently significant pathways affected by PM2.5, which play key roles in regulating cell proliferation, cell differentiation, cytoskeleton regulation, and inflammatory response. Finally, for the purpose of verifing the accuracy of microarray analysis, qRT-PCR was used to detect the expression of part key genes in the above signaling pathways, which were selected from the signal-net. Our study provided a large amount of information on the molecular mechanism that underling PM2.5 caused pulmonary diseases, and follow-up researches are still needed for further exploration.