Growth arrest specific-6 and angiotoxin receptor-like signaling drive oral regenerative wound repair.

ABSTRACT: Rapid and scarless wound repair is a hallmark of the oral mucosa, yet the cellular and molecular mechanisms that enable this regeneration remain unclear. By comparing populations of murine oral mucosal fibroblasts (OMFs) and facial skin fibroblasts (FSFs), we have identified mechanisms that facilitate regeneration over fibrosis. We found that OMFs used growth arrest specific-6 (GAS6)-angiotoxin receptor-like (AXL) signaling to suppress fibrosis-related mechanosignaling through focal adhesion kinase (FAK) in vitro. Inhibition or knockdown of AXL in the murine oral mucosa resulted in fibrotic wounds and increased activation of FAK. Stimulation of AXL by exogenous GAS6 in the murine facial skin yielded wounds that healed regeneratively as assessed by collagen deposition and organization. Rare

SUBMITTER: Griffin MF 

PROVIDER: S-EPMC12310197 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature