lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1

Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation.