Burns can impair the barrier function of the skin, and small burns can also cause high mortality. The WHO has described that over 180,000 people die of burns worldwide each year. Thus, the treatment of burn wounds is a major clinical challenge. Chitooligosaccharides (COS) are alkaline amino oligosaccharides with small molecular weights obtained by enzyme or chemical degradation of chitosan. With the characteristics of biocompatibility, water solubility and degradability, it has attracted increasing attention in the fields of biomedicine. In the present study, we used COS to treat deep second-degree burn wounds of rat skin and found that COS was able to promote wound healing. We also revealed that COS could promote fibroblast proliferation. Transcriptome sequencing analysis was performed on COS-treated fibroblasts to identify the underlying mechanisms. The results showed that COS was able to promote wound healing through regulation of the mitogen-activated protein kinase (MAPK) pathway and growth factor Hepatocyte Growth Factor (HGF). Our results provide a potential drug for burn wound therapy and the related molecular mechanism.
Keloid is a pathological result caused by cutaneous injury and irritation, which is on account of excessive deposition of collagen matrix and the growth of fibrous tissue. Long term and uncontrolled chronic inflammation is also one of the main causes. The mechanism of its formation is not clear. Therefore, in this study, we aimed to find key genes for diagnosis. We selected two datasets from the GEO database to find DGEs. Then, we finally obtained one gene, HOXC9, via WGCNA analysis and two algorithms (LASSO and SVM-RFE). Next, we analyzed its expression in normal tissues versus keloid and studied its change over time by Mfuzz time clustering analysis. Finally, through the analysis of this gene and previous studies we realized that, in addition to cell proliferation, immune infiltration also plays a role during the process of keloid formation, and we then explored the infiltration of immune cells in the normal versus keloid groups and the relationship between this gene and them.
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