β-Catenin-regulated myeloid cell adhesion and migration determine wound healing.
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.
Duke Scholars
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Related Subject Headings
- beta Catenin
- Wound Healing
- Transforming Growth Factor beta1
- Transcriptome
- TCF Transcription Factors
- Skin
- Myeloid Cells
- Mice, Transgenic
- Mice, Knockout
- Mice
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- beta Catenin
- Wound Healing
- Transforming Growth Factor beta1
- Transcriptome
- TCF Transcription Factors
- Skin
- Myeloid Cells
- Mice, Transgenic
- Mice, Knockout
- Mice