Abstract
Pressure therapy has been proved to be an effective treatment for hypertrophic scars in a clinical setting. However, evidence-based data are controversial and the precise mechanism of action of this technique remains unknown. The aim of this study was to investigate the potential molecular mechanisms of pressure therapy for hypertrophic scars. We established a Bama minipig (Sus scrofa) model of hypertrophic scarring in which the scars were treated with pressure to explore the mechanism of action of the treatment. There were 568 differentially expressed genes (289 upregulated, 279 downregulated) after pressure therapy at 90 days post-injury, whereas only 365 genes were differentially expressed (250 upregulated, 115 downregulated) at 120 days post-injury. These genes were associated with metabolic pathways, ECM-receptor interaction, the PI3K-Akt and MAPK signaling pathways, focal adhesion and cytokine-cytokine receptor interaction. In addition, the qRT-PCR results indicated that the trend of gene expression following pressure therapy was mostly consistent across the two methods. In conclusion, our systematic analysis of the transcriptome has provided a better understanding of the molecular mechanisms involved in pressure therapy and offers an important basis for further studies of the complex signaling pathways regulated by the treatment.