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

Autor(es)

Cogliati, Bruno ^[1] ; Vinken, Mathieu ^[2] ; Silva, Tereza C. ^[1] ; Araujo, Cintia M. M. ^[1] ; Aloia, Thiago P. A. ^[1] ; Chaible, Lucas M. ^[1] ; Mori, Claudia M. C. ^[1] ; Dagli, Maria L. Z. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Sch Vet Med & Anim Sci, Dept Pathol, BR-05508270 Sao Paulo - Brazil

^[2] Vrije Univ Brussel, Dept Vitro Toxicol & Dermato Cosmetol, Brussels - Belgium

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF DERMATOLOGICAL SCIENCE; v. 79, n. 1, p. 50-56, JUL 2015.
• Citações Web of Science: 19

Resumo

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. (C) 2015 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved. (AU)

• Processo FAPESP: 07/59764-9 - Avaliacao do processo cicatricial na pele de camundongos deficientes em conexina 43: enfoque no remodelamento da matriz extracelular.
• Beneficiário: Maria Lucia Zaidan Dagli
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 13/50420-6 - Canais de conexina e panexina como alvos terapêuticos e biomarcadores nas doenças hepáticas aguda e crônica
• Beneficiário: Mathieu Frederick Alexander Vinken
• Modalidade de apoio: Auxílio à Pesquisa - Programa SPEC