A Regulatory Loop between β-Catenin and Extra-cellular Matrix Components during the Proliferative Phase of Cutaneous Wound Healing

The study explored the regulatory relationship between β-Catenin and extracellular matrix (ECM) components during the proliferative phase of cutaneous wound healing. It was found that β-Catenin activation in dermal fibroblasts was enhanced by ECM components through an integrin-mediated, glycogen synthase kinase 3β dependent pathway. In vivo experiments with EDA-fibronectin deficient mice showed reduced β-Catenin signaling and impaired wound healing, which could be reversed by activating β-Catenin genetically or pharmacologically. This indicated that ECM components regulate β-Catenin activity, forming a regulatory loop that influences fibroblast behavior and wound properties. Microarray analysis identified new ECM targets of β-Catenin, suggesting a complex interaction that modulates wound repair.