Biphasic expression of stromal cell-derived factor-1 during human 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 exp...
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Published in | British journal of dermatology (1951) Vol. 157; no. 6; pp. 1148 - 1154 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.12.2007
Blackwell |
Subjects | |
Online Access | Get full text |
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Abstract | 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. |
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AbstractList | 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. 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. To elucidate expression of the multifunctional CXC chemokine SDF-1/CXCL12 during human wound healing. Skin biopsies were obtained from 14 volunteers between 1 and 21 days after incisional wounding and processed for in situ hybridization and immunohistochemistry. 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-alpha and interferon-gamma downregulated its expression in human dermal microvascular endothelial cells and fibroblasts. 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. BACKGROUNDChemokines 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.OBJECTIVESTo elucidate expression of the multifunctional CXC chemokine SDF-1/CXCL12 during human wound healing.METHODSSkin biopsies were obtained from 14 volunteers between 1 and 21 days after incisional wounding and processed for in situ hybridization and immunohistochemistry.RESULTSWe 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-alpha and interferon-gamma downregulated its expression in human dermal microvascular endothelial cells and fibroblasts.CONCLUSIONSOur 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. |
Author | Müller, V. Goebeler, M. Toksoy, A. Gillitzer, R. |
Author_xml | – sequence: 1 givenname: A. surname: Toksoy fullname: Toksoy, A. organization: Department of Dermatology, University of Würzburg, Würzburg, Germany – sequence: 2 givenname: V. surname: Müller fullname: Müller, V. organization: Department of Dermatology, University of Würzburg, Würzburg, Germany – sequence: 3 givenname: R. surname: Gillitzer fullname: Gillitzer, R. organization: Department of Dermatology, University of Würzburg, Würzburg, Germany – sequence: 4 givenname: M. surname: Goebeler fullname: Goebeler, M. organization: Department of Dermatology, University of Würzburg, Würzburg, Germany |
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Keywords | 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 |
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Snippet | Summary
Background Chemokines tightly regulate the spatial and temporal infiltration of invading leucocyte subsets during wound healing. Stromal cell‐derived... Chemokines tightly regulate the spatial and temporal infiltration of invading leucocyte subsets during wound healing. Stromal cell-derived factor-1... BACKGROUNDChemokines tightly regulate the spatial and temporal infiltration of invading leucocyte subsets during wound healing. Stromal cell-derived factor-1... |
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StartPage | 1148 |
SubjectTerms | 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 |
Title | Biphasic expression of stromal cell-derived factor-1 during human wound healing |
URI | https://api.istex.fr/ark:/67375/WNG-81GP7S29-T/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1365-2133.2007.08240.x https://www.ncbi.nlm.nih.gov/pubmed/17941943 https://search.proquest.com/docview/68524239 |
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