| Description |
Airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 um (PM2.5) associates with multiple airway diseases, which mainly ingests through the respiratory tract and is able to enter the lungs, extremely likely inducing pulmonary fibrosis. However, the precise molecular mechanisms of PM2.5-induced pulmonary fibrosis is the subject of intense investigation and currently poorly understood. Herein, we found that PM2.5 exposure leads to aberrant mRNA 5-methylcytosine (m5C) gain and loss in pulmonary fibrosis mouse lung. Further, we first show the m5C mediated regulatory map of gene ontology and protein protein interaction after PM2.5 exposure. atp5j2, atp5l, atpif1, ndufb6, chi3l1, lcn2, mmp9, adipoq, fgr, slc11a1 and tyrobp, which are highly enriched in oxidative stress response, inflammatory response and immune system process and act as m5C gain-upregulated factors, are critical for development of PM2.5-induced fibrosis in mouse lung. Our study manifests a novel mechanism of RNA m5C methylation-regulated PM2.5-induced pulmonary fibrosis development and paves the way for identification and application of potential biomarkers of lung injury after PM2.5 exposure in further study. |
