| First Author | Amini-Nik S | Year | 2014 |
| Journal | J Clin Invest | Volume | 124 |
| Issue | 6 | Pages | 2599-610 |
| PubMed ID | 24837430 | Mgi Jnum | J:212902 |
| Mgi Id | MGI:5582517 | Doi | 10.1172/JCI62059 |
| Citation | Amini-Nik S, et al. (2014) beta-Catenin-regulated myeloid cell adhesion and migration determine wound healing. J Clin Invest 124(6):2599-610 |
| abstractText | A beta-catenin/T cell factor-dependent transcriptional program is critical during cutaneous wound repair for the regulation of scar size; however, the relative contribution of beta-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 beta-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 beta-catenin exhibited insufficient skin wound healing due to macrophage-specific defects in migration, adhesion to fibroblasts, and ability to produce TGF-beta1. In irradiated mice, only macrophages expressing beta-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, beta-catenin levels, and cellularity. Our data indicate that beta-catenin regulates myeloid cell motility and adhesion and that beta-catenin-mediated macrophage motility contributes to the number of mesenchymal cells and ultimate scar size following cutaneous injury. |
