The pro-healing effect of exendin-4 on wounds produced by abrasion in normoglycemic mice

Eur J Pharmacol. 2015 Oct 5:764:346-352. doi: 10.1016/j.ejphar.2015.06.056. Epub 2015 Jul 8.

Abstract

Experimental evidence suggested that Exendin-4 (Exe4), an agonist at glucagon like receptor-1 (GLP-1R), promoted tissue regeneration. We aimed to verify the effect of Exe4, in the absence or in the presence of Exendin-4(9-39), an antagonist at GLP-1R, on the healing of abraded skin. Two wounds (approximately 1.1×1.1 cm(2); namely "upper" and "lower" in respect of the head) were produced by abrasion on the back of 12 mice, which were then randomly assigned to receive an intradermal injection (20 μl) of Group 1: saline (NT) or Exe4 (62 ng) in the upper and lower wound respectively; Group 2: Exendin-4(9-39) (70 ng) in the upper and Exendin-4(9-39) (70 ng) and, after 15 min, Exe4 (62 ng) in the lower wound. Wounds were measured at the time of abrasion (T0) and 144 h (T3) afterward taking pictures with a ruler and by using a software. The inflammatory cell infiltrate, fibroblasts/myofibroblasts, endothelial cells and GLP-1R expression, were each labeled by immunofluorescence in each wound, pERK1/2 was evaluated by Western-blot in wound lysates. At T3, the percentage of healing surface was 53% and 92% for NT and Exe4 wounds respectively and 68% and 79% for those treated with Exendin-4(9-39) and Exendin-4(9-39)+Exe4 respectively. Exe4, but not Exendin-4(9-39) induced quantitative increase in fibroblasts/myofibroblasts and vessel density when compared to NT wounds. This increase was not evident in wounds treated with Exendin-4(9-39)+Exe4. Exe4 promotes wound healing opening to the possible dermatological use of this incretin analogue.

Keywords: Angiogenesis; Exendin-4; Exendin-4(9-39); Glucagon-like type 1 receptor; Wound healing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Proliferation / drug effects
  • Cell Transdifferentiation / drug effects
  • Dermatologic Agents / pharmacology*
  • Disease Models, Animal
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology
  • Enzyme Activation
  • Exenatide
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Glucagon-Like Peptide-1 Receptor / agonists
  • Glucagon-Like Peptide-1 Receptor / antagonists & inhibitors
  • Glucagon-Like Peptide-1 Receptor / metabolism
  • Incretins / pharmacology*
  • Male
  • Mice
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Myofibroblasts / drug effects
  • Myofibroblasts / metabolism
  • Myofibroblasts / pathology
  • Peptide Fragments / pharmacology
  • Peptides / pharmacology*
  • Phosphorylation
  • Skin / drug effects*
  • Skin / injuries
  • Skin / metabolism
  • Skin / pathology
  • Time Factors
  • Venoms / pharmacology*
  • Wound Healing / drug effects*
  • Wounds and Injuries / drug therapy*
  • Wounds and Injuries / metabolism
  • Wounds and Injuries / pathology

Substances

  • Dermatologic Agents
  • Glp1r protein, mouse
  • Glucagon-Like Peptide-1 Receptor
  • Incretins
  • Peptide Fragments
  • Peptides
  • Venoms
  • exendin (9-39)
  • Exenatide
  • Mapk1 protein, mouse
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3