ATAC-seq between normal skin and wound edge epidermis in Hdac5fl/fl and K14cre;Hdac5fl/fl mice

Re-epithelialization is a crucial process in skin wound healing. To date, the underlying mechanisms of re-epithelialization remain elusive, and effective strategies have not yet been developed. Histone deacetylase 5 (HDAC5), classified as a class IIa HDAC protein, primarily modulates chromatin accessibility and regulates transcriptional activity through deacetylating lysine residues on core histones. Additionally, it engages in interactions with several transcription factors, notably the extensively researched myocyte enhancer factor 2 (MEF2), influencing the expression of MEF2-dependent genes. Beyond histone proteins, HDAC5 has exhibited non-histone deacetylase activity, targeting substrates like tubulin and p65. Given that the successful activation of silent genes is pivotal for an effective regeneration process, the regulatory role of HDAC5 in the transcription of genes associated with regeneration underscores its potential in wound repair. Therefore, in this study, we investigated the differences in gene expression in the skins of hdac5 conditional knockout mice and their wild-type littermates under normal conditions and after wounding. Overall design: To explore the influence of HDAC5 both normal skin and wound edge, we developed a model utilizing epidermal Hdac5 gene conditional knock-out K14cre;Hdac5fl/fl mice. Employing the excisional wound splinting model, we procured the wound edge specimens for analysis.