Identification of mitochondrial function-associated lncRNAs in septic mice myocardium

The present study aimed to analyze long noncoding RNA (lncRNA) and messenger RNA (mRNA) expression profiles in septic mice heart and to identify potential lncRNAs and mRNAs that be responsible for cardiac mitochondrial dysfunction during sepsis. Mice were treated with 10 mg/kg of lipopolysaccharides to induce sepsis. LncRNAs and mRNAs expression were evaluated by using lncRNA and mRNA microarray or real-time polymerase chain reaction technique. LncRNA-mRNA coexpression network assay, Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed. The results showed that 1275 lncRNAs were differentially expressed in septic myocardium compared with those in the control group. A total of 2769 mRNAs were dysregulated in septic mice heart, most of which are mainly related to the process of inflammation, mitochondrial metabolism, oxidative stress, and apoptosis. Coexpression network analysis showed that 14 lncRNAs were highly correlated with 11 mitochondria-related differentially expressed mRNA. Among all lncRNAs and theircis-acting mRNAs, 41 lncRNAs-mRNA pairs (such as NONMMUG004378 andApaf1gene) were enriched in GO terms and KEGG pathways. In summary, we gained some specific lncRNAs and their potential target mRNAs that might be involved in mitochondrial dysfunction in septic myocardium. These findings provide a panoramic view of lncRNA and might allow developing new treatment strategies for sepsis.

Automated summary

This study analyzed the expression profiles of lncRNAs and mRNAs in septic mice hearts, identifying specific lncRNAs and mRNAs potentially responsible for cardiac mitochondrial dysfunction during sepsis. The dysregulation of numerous lncRNAs and mRNAs related to inflammation, mitochondrial metabolism, oxidative stress, and apoptosis in septic hearts was observed. Coexpression network analysis revealed potential interactions between lncRNAs and mitochondria-related mRNAs, providing insights into the molecular mechanisms underlying cardiac dysfunction in sepsis.