A Regulatory Loop Between β-Catenin and Extracellular 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 mice lacking the EDA-fibronectin variant showed reduced β-Catenin signaling, fewer fibroblasts, and weaker wounds, which were improved by activating β-Catenin genetically or with Lithium Chloride. This indicated that ECM components regulate β-Catenin activity, which in turn modulates cell behavior and wound properties. The study also identified new ECM targets of β-Catenin through microarray analysis, suggesting a regulatory loop between β-Catenin and ECM components in wound repair.