Integrated analysis of ATAC-seq and RNA-seq reveals ADSCP2 regulates oxidative phosphorylation pathway in hypertrophic scar fibroblasts.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The primary effector cells involved in the formation of hypertrophic scars are fibroblasts. A potential peptide, ADSCP2 (adipose-derived stem cell peptide 2, the peptide fragment of ALCAM protein), derived from adipose-derived stem cell-conditioned medium, has been identified as having the potential to mitigate hypertrophic scar formation by targeting pyruvate carboxylase. However, the underlying mechanisms remain incompletely understood. Whether ADSCP2 attenuates hypertrophic scar fibrosis at the transcription level remains unclear. Consequently, this study sought to elucidate the potential mechanism associated with ADSCP2 by examining genome-wide transcriptional alterations and changes in chromatin accessibility in fibroblasts. This was achieved through the integrated analysis of assay for transposase accessible chromatin using sequencing (ATAC-seq) and RNA sequencing (RNA-seq). In the ADSCP2 treatment group, ATAC-seq identified a total of 7,805 differential peaks associated with 3,176 genes. RNA-seq analysis revealed 345 upregulated and 399 downregulated transcripts in the same group. A combined Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of both downregulated genes and close-ACRs (accessible chromatin regions) genes within the ADSCP2 treatment group indicated regulation of the oxidative phosphorylation pathway (OXPHOS) by ADSCP2. The amalgamat

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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