Connexin 43 deficiency accelerates skin wound healing and extracellular matrix remodeling in mice. Issue 1 (July 2015)

• Record Type: Journal Article
• Authors: Cogliati, Bruno; Vinken, Mathieu; Silva, Tereza C.; Araújo, Cintia M.M.; Aloia, Thiago P.A.; Chaible, Lucas M.; Mori, Cláudia M.C.; Dagli, Maria L.Z.
• Is Part Of: Journal of dermatological science. Volume 79:Issue 1(2015:Jul.)
• Page Start: 50
• Page End: 56
• Publication Date: 2015-07
• Subjects: Connexin 43 -- Gap junction -- Skin repair -- Wound healing; Dermatology -- Periodicals; Skin Diseases -- Periodicals; Dermatologie -- Périodiques; 616.5005
• DOI: 10.1016/j.jdermsci.2015.03.019
• Languages: English
• ISSNs: 0923-1811

Abstract

Highlights: Cx43 deficiency accelerates re-epithelialization and wound closure. Cx43 deficiency increases proliferation and activation of dermal fibroblasts. Cx43 deficiency enhances the expression of extracellular matrix remodeling factors. Cx43 may contribute to the development of new therapeutic target in wound healing. 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.