Highly expressed TRIM32 promoted traumatic wound healing by mediating ubiquitination of PIAS1

Abstract

Poor wound healing is a significant challenge that can result in lower limb amputation. Unfortunately, effective treatments are currently limited. Therefore, there is an urgent need to investigate new targets within the skin healing process to identify more effective treatment options. Differentially expressed genes (DEGs) were identified before and after wound healing based on the gene expression profiles GSE23006 and GSE21648 from the Gene Expression Omnibus database, and enrichment analysis of the DEGs was performed. And we found that a total of three differentially expressed genes (DEGs)-TFPI2, ELN, and TRIM32-were identified as key genes in the wound healing process. TRIM32 was selected for further study due to its high expression levels and significant variance in expression in an in vitro wound healing model. The overexpression of TRIM32 promoted skin fibroblast cells migration and epithelial-mesenchymal transition (EMT). Mechanistically, TRIM32 regulated the ubiquitination of PIAS1, leading to a reduction in PIAS1 protein expression. Additionally, TRIM32 has been shown to enhance wound healing by modulating PIAS1 expression. These findings highlight the beneficial role of TRIM32 in wound healing and tissue repair, suggesting that the TRIM32/PIAS1 axis may serve as a promising therapeutic target for enhancing wound healing.