?-Catenin-regulated myeloid cell adhesion and migration determine wound healing.

ABSTRACT: A ?-catenin/T cell factor-dependent transcriptional program is critical during cutaneous wound repair for the regulation of scar size; however, the relative contribution of ?-catenin activity and function in specific cell types in the granulation tissue during the healing process is unknown. Here, cell lineage tracing revealed that cells in which ?-catenin is transcriptionally active express a gene profile that is characteristic of the myeloid lineage. Mice harboring a macrophage-specific deletion of the gene encoding ?-catenin exhibited insufficient skin wound healing due to macrophage-specific defects in migration, adhesion to fibroblasts, and ability to produce TGF-?1. In irradiated mice, only macrophages expressing ?-catenin were able to rescue wound-healing deficiency. Evaluation of scar tissue collected from patients with hypertrophic and normal scars revealed a correlation between the number of macrophages within the wound, ?-catenin levels, and cellularity. Our data indicate that ?-catenin regulates myeloid cell motility and adhesion and that ?-catenin-mediated macrophage motility contributes to the number of mesenchymal cells and ultimate scar size following cutaneous injury.

SUBMITTER: Amini-Nik S 

PROVIDER: S-EPMC4089463 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature