miR-29b promotes skin wound healing and reduces excessive scar formation by inhibition of the TGF-β1/Smad/CTGF signaling pathway

Can J Physiol Pharmacol. 2017 Apr;95(4):437-442. doi: 10.1139/cjpp-2016-0248. Epub 2016 Nov 24.

Abstract

The hypertrophic scar is a medical difficulty of humans, which has caused great pain to patients. Here, we investigated the inhibitory effect of miR-29b on scar formation. The scalded model was established in mice and miR-29b mimics or a negative control was subcutaneously injected into the injury skin. Then various molecular biological experiments were performed to assess the effect of miR-29b on scar formation. According to our present study, first, the results demonstrated that miR-29b was down-regulated in thermal injury tissue and miR-29b treatment could promote wound healing, inhibit scar formation, and alleviate histopathological morphologic alteration in scald tissues. Additionally, miR-29b treatment suppressed collagen deposition and fibrotic gene expression in scar tissues. Finally, we found that miR-29b treatment inhibited the TGF-β1/Smad/CTGF signaling pathway. Taken together, our data suggest that miR-29b treatment has an inhibitory effect against scar formation via inhibition of the TGF-β1/Smad/CTGF signaling pathway and may provide a potential molecular basis for future treatments for hypertrophic scars.

Keywords: CTGF; Smad2/3; TGF-β1; formation de cicatrices; miR-29b; scar formation.

MeSH terms

  • Animals
  • Cicatrix, Hypertrophic / metabolism
  • Cicatrix, Hypertrophic / therapy*
  • Collagen / metabolism*
  • Connective Tissue Growth Factor / metabolism
  • Disease Models, Animal
  • Down-Regulation
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / metabolism
  • MicroRNAs / therapeutic use*
  • Molecular Targeted Therapy
  • Signal Transduction
  • Smad Proteins, Receptor-Regulated / metabolism
  • Transforming Growth Factor beta1 / metabolism
  • Wound Healing*

Substances

  • CCN2 protein, mouse
  • MIRN29 microRNA, mouse
  • MicroRNAs
  • Smad Proteins, Receptor-Regulated
  • Tgfb1 protein, mouse
  • Transforming Growth Factor beta1
  • Connective Tissue Growth Factor
  • Collagen