Biphasic expression of stromal cell-derived factor-1 during human wound healing

• Published in: British journal of dermatology (1951) Vol. 157; no. 6; pp. 1148 - 1154
• Main Authors: Toksoy, A., Müller, V., Gillitzer, R., Goebeler, M.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.12.2007; Blackwell
• Subjects: Adult; Biological and medical sciences; Cell Movement; Cells, Cultured; Chemokine CXCL12 - metabolism; chemokines; Chemokines, CXC - biosynthesis; Chemokines, CXC - genetics; CXCL12; CXCR4; Dermatology; endothelial cells; Endothelial Cells - metabolism; Female; Fibroblasts - metabolism; Humans; Male; Medical sciences; RNA, Messenger - metabolism; stromal cell-derived factor-1; Stromal Cells - metabolism; Tumor Necrosis Factor-alpha - metabolism; wound healing; Wound Healing - physiology; Human; Endothelial cell; endothelial cells; wound healing; Dermatology; CXCR4; chemokines; Wound; Stromal cell derived factor 1; CXCL12; Healing agent; CXC chemokine; stromal cell-derived factor-1; Cicatrization
• ISSN: 0007-0963; 1365-2133
• DOI: 10.1111/j.1365-2133.2007.08240.x

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.