LncRNA and mRNA m6A modification profile and functional network in sepsis-induced acute lung injury.

N6-methyladenosine (m6A) modification is crucial in sepsis-related organ damage, but its profiles in sepsis-induced acute lung injury (ALI) remain unclear. In this study, we elucidated the landscape and network of m6A modification in a rat model of lipopolysaccharide (LPS)-induced ALI. Total m6A levels in lung tissues from control and LPS-treated rats were determined using liquid chromatography tandem mass spectrometry. Epitranscriptomic microarray identified differentially m6A-modified mRNAs and long non-coding RNAs (lncRNAs). Bioinformatic analyses were performed to explore the functional implications of these differentially methylated transcripts. Selected methylated lncRNAs were further validated using m6A single-base site quantitative PCR. Results indicated significantly reduced total m6A levels in lung tissues from LPS-treated rats. 283 mRNAs showed decreased m6A modification levels and were enriched in immune response and inflammation pathways. Among the differentially expressed lncRNAs, LOC102551452 displayed m6A hypomethylation and negative correlation with neutrophil-related genes. These findings illuminate the potential role of m6A modification in immune and inflammation processes during sepsis-induced ALI, suggesting that targeting m6A modifications could be a potential therapeutic approach for sepsis-induced ALI.