The effects of pressure intervention on wound healing and scar formation in a Bama minipig model

Burns. 2019 Mar;45(2):413-422. doi: 10.1016/j.burns.2018.09.002. Epub 2018 Sep 28.

Abstract

Pressure therapy has been widely used in clinical practice for the prevention or treatment of hypertrophic scars resulted from aberrations in wound healing. However, the precise molecular mechanisms of this process are only partially understood. In the present study, we established a Bama minipig model to observe the effect of pressure intervention on wound healing and scar formation. Transcriptome sequencing was performed to analyze the gene expression profiles in the injured and pressure-treated tissues. Furthermore, expression of the critical factors associated with IGF-1/IGF-1R pathways including PI3K/AKT and MEK/ERK and collagens were further analyzed by quantitative polymerase chain reaction (q-PCR) and Western blot. We observed that the mRNA expression of IGF-1 and IGF-1R were down-regulated in the pressure treated groups. Following pressure intervention, the trend in expression of PI3K/AKT decreased, whereas that of MEK/ERK expression increased, when quantified by q-PCR. Moreover, the level of PI3K protein expression decreased significantly after pressure treatment for one month but there was no significant difference in AKT protein expression. Interestingly, the trend in MEK/ERK protein expression was opposite to that indicated by q-PCR analysis. Furthermore, collagen I and III mRNA clearly declined after one month pressure treatment. Taken together, these results indicated that pressure intervention alleviated scar formation may via inhibiting the IGF-1/IGF-1R signaling pathway and collagen expression in the Bama minipig model.

Keywords: IGF-1/IGF-1R; Pressure; Scars; Signaling pathway.

MeSH terms

  • Animals
  • Burns / genetics*
  • Burns / pathology
  • Burns / therapy
  • Cicatrix / genetics*
  • Cicatrix / pathology
  • Cicatrix / prevention & control
  • Cicatrix, Hypertrophic / genetics*
  • Cicatrix, Hypertrophic / pathology
  • Cicatrix, Hypertrophic / prevention & control
  • Collagen Type I / genetics
  • Collagen Type III / genetics
  • Extracellular Signal-Regulated MAP Kinases / genetics
  • Female
  • Insulin-Like Growth Factor I / genetics
  • Phosphatidylinositol 3-Kinases / genetics
  • Pressure*
  • Proto-Oncogene Proteins c-akt / genetics
  • RNA, Messenger / metabolism
  • Receptor, IGF Type 1 / genetics
  • Signal Transduction
  • Swine
  • Swine, Miniature
  • Wound Healing*

Substances

  • Collagen Type I
  • Collagen Type III
  • RNA, Messenger
  • Insulin-Like Growth Factor I
  • Receptor, IGF Type 1
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases