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

Published

Journal Article

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. Our 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.

Full Text

Duke Authors

Cited Authors

  • Amini-Nik, S; Cambridge, E; Yu, W; Guo, A; Whetstone, H; Nadesan, P; Poon, R; Hinz, B; Alman, BA

Published Date

  • June 2014

Published In

Volume / Issue

  • 124 / 6

Start / End Page

  • 2599 - 2610

PubMed ID

  • 24837430

Pubmed Central ID

  • 24837430

Electronic International Standard Serial Number (EISSN)

  • 1558-8238

Digital Object Identifier (DOI)

  • 10.1172/JCI62059

Language

  • eng

Conference Location

  • United States