[Beta]-Catenin-regulated myeloid cell adhesion and migration determine wound healing

• Published in: The Journal of clinical investigation 2014-06, Vol.124 (6), p.2599
• Main Authors: Amini-Nik, Saeid, Cambridge, Elizabeth, Yu, Winston, Guo, Anne, Whetstone, Heather, Nadesan, Puviindran, Poon, Raymond, Hinz, Boris, Alman, Benjamin A
• Format: Article
• Language: English
• Subjects: Biomedical research; Bone marrow; Cell adhesion & migration; Kinases; Medical research; Wound healing
• ISSN: 0021-9738; 1558-8238

A β-catenin/T cell factor-dependent transcriptional program is critical during cutaneous wound repair for the regulation of scar size; however, the relative contribution of β-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 β-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 β-catenin exhibited insufficient skin wound healing due to macrophage-specific defects in migration, adhesion to fibroblasts, and ability to produce TGF-β1. In irradiated mice, only macrophages expressing β-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, β-catenin levels, and cellularity. The authors data indicate that, β-catenin regulates myeloid cell motility and adhesion and that β-catenin-mediated macrophage motility contributes to the number of mesenchymal cells and ultimate scar size following cutaneous injury.