Hydrogen sulfide exposure induces apoptosis and necroptosis through lncRNA3037/miR-15a/BCL2-A20 signaling in broiler trachea

Hydrogen sulfide (H2S) is an air pollutant, has toxic effects on respiratory tract. However, the underlying mechanisms of H2S induced respiratory toxicity and the roles of long non-coding RNAs (lncRNA) and microRNA (miRNA) in this process remain poorly understood. To clear this, we investigated the change of tracheal tissue ultrastructure and the expression profiles of lncRNAs and miRNAs of chicken trachea exposed to H2S for 42 days. Results showed that H2S exposure triggered apoptosis, necroptosis, and differential expression of 16 lncRNAs and 18 miRNAs in broiler tracheas. The results of LMH cells stimulated by NaHS in vitro also showed the occurrence of apoptosis and necroptosis. LncRNA3037 is down-regulated and miR-15a is up-regulated in tracheal tissue and LMH cells under H2S exposure. Bioinformatics analysis and dual luciferase reporter system showed lncRNA3037 bound directly to miR-15a and negatively regulates each other. A20 and BCL2 are the target genes of miR-15a and negatively regulated by it. Overexpression of miR-15a caused apoptosis and necroptosis and its inhibition partially reversed apoptosis and necroptosis of LMH cells caused by NaHS stimulation and lncRNA3037 knockdown. Taken together, we concluded that H2S exposure mediates apoptosis and necroptosis through lncRNA3037/miR-15/A20-BCL2. These results provide new insights for unveiling the biological effects of H2S in vivo and in vitro. [Display omitted] •H2S exposure induces apoptosis and necroptosis in broiler trachea.•H2S exposure causes changes in the miRNA and lncRNA profiles of broiler trachea.•LncRNA3037 is a molecular sponge of miR-15a.•LncRNA3037/miR-15/A20-BCL2 signaling contributes to trachea injury caused by H2S.