Atmospheric fine particle pollution is known to cause many adverse health effects. However, the potential mechanisms of PM2.5-induced cytotoxicity still needs further understanding. Herein, we integrated cytotoxicity, component profiling, metabolomics and proteomics data to deeply explain the biological responses of human bronchial epithelial cells exposed to PM2.5. We observed that PM2.5 caused cell cycle arrest, calcium influx, cell damage and further induced cell apoptosis. The contents of heavy metals and 4-6 rings PAHs in PM2.5 were positively correlated with intracellular ROS, indicating that they might be the important components to induce the above cytotoxicity. Integrated metabolomics and proteomics analysis revealed the significant alterations of many metabolic processes, such as glycolysis, the citric acid cycle, amino acid metabolism and lipid metabolism. Notably, we found that PM2.5 inhibited the integrin signaling pathway, including down-regulating the protein expression of integrins and the phosphorylation of downstream signaling kinases, which might ultimately affect cell cycle progression, cell metabolism and apoptosis. This study provided a comprehensive data resource for the deep understanding of biological toxicity mechanisms caused by atmospheric fine particles in human lung-bronchial epithelium cells.
Keywords: Cytotoxicity; Integrin; Metabolomics; PM(2.5); Proteomics.
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