Histone modification in the lung injury and recovery of mice in response to PM2.5 exposure
2019
Ji, Xiaotong | Yue, Huifeng | Ku, Tingting | Zhang, Yingying | Yun, Yang | Li, Guangke | Sang, Nan
Epidemiological and experimental studies have progressively provided a better knowledge of the underlying mechanisms by which fine particulate matter (PM₂.₅) exerts its harmful health effects. However, limited studies focused on the effect and following recovery after the particulate exposure ended. In this study, we determined PM₂.₅ exposure-caused effects on the lung and their recovery in mice after terminating aspiration, and clarified the possible molecular modification. The results revealed that PM₂.₅ exposure for 4 weeks significantly decreased the lung function, and the changes returned to normal levels after 1-week recovery. However, we observed persistent particle alveolar load following 2-week recovery. Interestingly, the alterations of H3K27ac expression and related enzyme activities mimicked the changes of respiratory function during the process, and chromatin immunoprecipitation-seqences (ChIP-seq) suggested that these PM₂.₅-associated differential H3K27ac markers participated in immune responses and chemokine signaling pathway with stat2 and bcar1 being two important genes. Consistently, the expression of pro-inflammatory cytokines and chemokines elevated after PM₂.₅ exposure for 4-week, and reversed to normal levels following 2-week recovery. The study highlighted that PM₂.₅ aspiration caused histone modification associated lung dysfunction and inflammation, and the action restored after exposure ending and 2-week recovery. Also, persistent particle alveolar load might be a long-term potential risk for lung diseases.
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