Fine particulate matter 2.5 exerted its toxicological effect by regulating a new layer, long non-coding RNA.

Fine particulate matter (PM2.5) exposure, especially to its organic components, induces adverse health effects on the respiratory system. However, the molecular mechanisms have still not been fully elucidated. Long non-coding RNA (lncRNA) is involved in various physio-pathological processes. In this study, the roles of lncRNA were investigated to reveal the toxicology of PM2.5. Organic extracts of PM2.5 from Nanjing and Shanghai cities were adopted to treat human bronchial epithelial cell lines (BEAS-2B and A549). RNA sequencing showed that the lncRNA functioned as antisense RNA, intergenic RNA and pre-miRNA. The mRNA profiles were also altered after exposure. PM2.5 from Nanjing showed a more serious impact than that from Shanghai. In detail, higher expression of n405968 was positively related to the elevated mRNA levels of inflammatory factors (IL-6 and IL-8). Increasing levels of metastasis associated lung adenocarcinoma transcript 1 (MALAT1) were positively associated with the induced epithelial-mesenchymal transition (EMT) process. Similar response was observed between both cell lines. The higher content of polycyclic aromatic hydrocarbons (PAHs) is likely to contribute to higher toxicity of PM2.5 from Nanjing than that from Shanghai. Antagonism of aryl hydrocarbon receptor (AHR) or inhibition of CYP1A1 diminished the effects stimulated by PM2.5. Our results indicated that lncRNAs could be involved in the toxicology of PM2.5 through regulating the inflammation and EMT process.