Characterization of the Chromatin Accessibility in the Hearts of Mice With Lipopolysaccharide (LPS)-Induced Sepsis.

This study investigates the transcription and expression of genes associated with Sepsis-induced cardiac dysfunction (SICD) in a sepsis mouse model by examining chromatin accessibility. The assay for transposase-accessible chromatin by sequencing (ATAC-seq) was employed to investigate chromatin reshaping associated with SICD in the sepsis mouse model. ATAC-seq data were generated from the hearts of sepsis mice, and the relationship between chromatin accessibility and gene expression was analyzed in conjunction with RNA sequencing. RNA-seq results indicated that the most differentially expressed genes were present 1 day post-induction. We identified 2389 increased and 5065 decreased sepsis-associated chromatin-accessible regions in the heart tissues of sepsis mice. At 1 day post-induction, 877 genes were upregulated, and 881 were downregulated. Notably, an enhanced ATAC-seq signal was observed in approximately 1311 genes, with 93 showing upregulated mRNA levels. The signatures of numerous transcription factors, including ERG, ETV2, Mef2c, and JunB, were enriched in the SICD-associated accessible chromatin regions. This study demonstrates that alterations in chromatin accessibility may serve as an initial mechanism in sepsis-induced cardiac dysfunction.