Connexin 43 deficiency accelerates skin wound healing and extracellular matrix remodeling in mice

J Dermatol Sci. 2015 Jul;79(1):50-56. doi: 10.1016/j.jdermsci.2015.03.019. Epub 2015 Apr 9.

Abstract

Background: Cellular channels composed of connexin 43 are known to act as key players in the life cycle of the skin and consequently to underlie skin repair.

Objective: This study was specifically set up to investigate the suite of molecular mechanisms driven by connexin 43-based channels on wound healing.

Methods: To this end, a battery of parameters, including re-epithelialization, neovascularization, collagen deposition and extracellular matrix remodeling, was monitored over time during experimentally induced skin repair in heterozygous connexin 43 knockout mice.

Results: It was found that connexin 43 deficiency accelerates re-epithelialization and wound closure, increases proliferation and activation of dermal fibroblasts, and enhances the expression of extracellular matrix remodeling mediators.

Conclusion: These data substantiate the notion that connexin 43 may represent an interesting therapeutic target in dermal wound healing.

Keywords: Connexin 43; Gap junction; Skin repair; Wound healing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Proliferation
  • Collagen / metabolism*
  • Connexin 43 / deficiency*
  • Connexin 43 / genetics
  • Extracellular Matrix / metabolism*
  • Fibroblasts / physiology
  • Heterozygote
  • Male
  • Mice
  • Mice, Knockout
  • Neovascularization, Physiologic
  • Re-Epithelialization / physiology*

Substances

  • Connexin 43
  • Collagen