lncRNA Gm16410 Mediates PM2.5-Induced Macrophage Activation via PI3K/AKT Pathway

PM₂.₅ refers to atmospheric particulate matters with a diameter of less than 2.5 μm. The deposit of PM₂.₅ in lung cells can cause oxidative stress, leading to changes in macrophage polarity, which can subsequently cause pulmonary inflammation. Long-chain non-coding RNA (lncRNA) is a class of transcripts that regulate biological processes through multiple mechanisms. However, the role of lncRNA in PM₂.₅-induced lung inflammation has not been established. In this study, the biological effects and associated mechanism of lncRNA in PM₂.₅-induced change in macrophage polarity were investigated. The lncRNA-mediated PM₂.₅-induced macrophage inflammation and lung inflammation-associated injury were also determined. Mice were exposed to chronic levels of PM₂.₅, and changes in the expression of lncRNA in the lung were measured by lncRNA microarray. lncRNAs that showed significant changes in expression in response to PM₂.₅ were identified. lncRNA showing the biggest change was subjected to further analysis to determine its functional roles and mechanisms with respect to macrophage activation. The result showed that a significant reduction in expression of one lncRNA, identified as lncGm16410, was observed in the lung of mice and RAW264.7 cells following exposure to PM₂.₅. lncGm16410 suppressed PM₂.₅-induced macrophage activation via the Src protein-mediated PI3K/Akt signaling pathway. PM₂.₅ promoted lung inflammation by downregulating the expression of lncGm16410, enhancing the activation of macrophages. Thus, lncGm16410 might provide new insight into the prevention of PM₂.₅ injury.