Conflicts of interest None declared.
1365-2133/asset/olbannerleft.jpg?v=1&s=3d13800721e0d35da4d49e694f63a9d81054ca17)
1365-2133/asset/olbannerright.jpg?v=1&s=9ea9b247f2d7101244b2bef959a0874a886ec363)
Biphasic expression of stromal cell-derived factor-1 during human wound healing
Article first published online: 18 OCT 2007
DOI: 10.1111/j.1365-2133.2007.08240.x
Additional Information
How to Cite
Toksoy, A., Müller, V., Gillitzer, R. and Goebeler, M. (2007), Biphasic expression of stromal cell-derived factor-1 during human wound healing. British Journal of Dermatology, 157: 1148–1154. doi: 10.1111/j.1365-2133.2007.08240.x
Publication History
- Issue published online: 18 OCT 2007
- Article first published online: 18 OCT 2007
- Accepted for publication 11 July 2007
- Abstract
- Article
- References
- Cited By
Keywords:
- chemokines;
- CXCL12;
- CXCR4;
- endothelial cells;
- stromal cell-derived factor-1;
- wound healing
Summary
Background Chemokines tightly regulate the spatial and temporal infiltration of invading leucocyte subsets during wound healing. Stromal cell-derived factor-1 (SDF-1/CXCL12) is a homeostatic chemokine with multiple functions; its role during cutaneous wound healing, however, needs to be explored.
Objectives To elucidate expression of the multifunctional CXC chemokine SDF-1/CXCL12 during human wound healing.
Methods Skin biopsies were obtained from 14 volunteers between 1 and 21 days after incisional wounding and processed for in situ hybridization and immunohistochemistry.
Results We analysed the spatial and temporal distribution of SDF-1/CXCL12 after artificial wounding and detected a complete downregulation at both the mRNA and the protein level within the fibrous stroma that replaces the initial wound defect. However, increased levels of SDF-1/CXCL12 were observed at the wound margins. Focusing on mediators regulating SDF-1/CXCL12 expression in vitro we realized that both tumour necrosis factor-α and interferon-γ downregulated its expression in human dermal microvascular endothelial cells and fibroblasts.
Conclusions Our data suggest that SDF-1/CXCL12 is tightly regulated during wound repair. Increased expression at the wound margin may contribute to the accumulation of endothelial progenitor cells, thus accelerating neovascularization.