miR‐24‐3p obstructs the proliferation and migration of human skin fibroblasts after thermal injury by targeting PPAR‐β and positively regulated by NF‐κB.

Thermal injury repair is a complex process during which the maintenance of the proliferation and migration of human skin fibroblasts (HSFs) exert a crucial role. MicroRNAs have been proven to exert an essential function in repairing skin burns. This study delves into the regulatory effects of miR‐24‐3p on the migration and proliferation of HSFs that have sustained a thermal injury, thereby, providing deeper insight into thermal injury repair pathogenesis. The PPAR‐β protein expression level progressively increased in a time‐dependent manner on the 12th, 24th and 48th hour following the thermal injury of the HSFs. The knockdown of PPAR‐β markedly suppressed the proliferation of and migration of HSF. Following thermal injury, the knockdown also promoted the inflammatory cytokine IL‐6, TNF‐α, PTGS‐2 and P65 expression. PPAR‐β contrastingly exhibited an opposite trend. A targeted relationship between PPAR‐β and miR‐24‐3p was predicted and verified. miR‐24‐3p inhibited thermal injured HSF proliferation and migration and facilitated inflammatory cytokine expression through the regulation of PPAR‐β. p65 directly targeted the transcriptional precursor of miR‐24 and promoted miR‐24 expression. A negative correlation between miR‐24‐3p expression level and PPAR‐β expression level in rats' burnt dermal tissues was observed. Our findings reveal that miR‐24‐3p is conducive to rehabilitating the denatured dermis, which may be beneficial in providing effective therapy of skin burns. [ABSTRACT FROM AUTHOR]