Downregulation of miR-27b promotes skin wound healing in a rat model of scald burn by promoting fibroblast proliferation

The aim of the present study was to investigate the effect and mechanism of action of microRNA (miR)-27b on skin wound healing in rats with deep second-degree scald burns and in BJ human skin fibroblast cells. Rat models with deep second-degree scald burns were constructed and injected with miR-27b mimics and inhibitors at the wound site daily for 21 days. Healing of burned skin tissues was observed at 0, 3, 7, 14 and 21 days following modeling. H&E and Masson staining were used to observe the pathological structure and degree of collagen fibers in the burned skin tissues. The effects of miR-27b on BJ cell proliferation and migration were determined by MTT and scratch assays. Matrix metalloproteinase-1 (MMP-1), alpha -smooth muscle actin (alpha -SMA), collagen I and collagen III expression in rat skin tissues and BJ cells were measured via reverse transcription-quantitative PCR and western blot analysis. The results of the in vivo experiments demonstrated that miR-27b inhibition accelerated scalded skin healing and induced fibroblast growth. Furthermore, the in vitro experiments revealed that miR-27b inhibition increased BJ cell proliferation and migration. Furthermore, miR-27b inhibition upregulated MMP-1, alpha -SMA, collagen I and collagen III expression in the skin tissues and cells, while the overexpression of miR-27b demonstrated the opposite effect. In conclusion, the results of the present study revealed that miR-27b inhibition increased fibroblast proliferation, thereby accelerating scald wound healing in rats.