Suppressed inflammatory gene expression during human hypertrophic scar compared to normotrophic scar formation
Autor: | Susan Gibbs, Etty H. de Jong, Lenie J. van den Broek, Frank B. Niessen, Willem M. van der Veer |
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Přispěvatelé: | Oral Cell Biology, Orale Celbiologie (ORM, ACTA), Dermatology, Plastic, Reconstructive and Hand Surgery, CCA - Immuno-pathogenesis, MOVE Research Institute |
Rok vydání: | 2015 |
Předmět: |
Pathology
Angiogenesis Biopsy hypertrophic Biochemistry normotrophic 14-3-3 PROTEINS Pathogenesis Extracellular matrix Postoperative Complications Angiogenic Proteins Extracellular Matrix Proteins CXCL2 CHEMOKINES Cytokines DERMAL FIBROBLASTS Tumor necrosis factor alpha medicine.symptom Inflammation Mediators medicine.medical_specialty Cicatrix Hypertrophic CCL3 Neovascularization Physiologic Inflammation Dermatology Real-Time Polymerase Chain Reaction scar Hypertrophic scar Cicatrix SDG 3 - Good Health and Well-being medicine Humans human BURN SCARS Molecular Biology Wound Healing business.industry GROWTH-FACTOR-BETA Macrophages KELOIDS CDNA MICROARRAYS KERATINOCYTES medicine.disease Sternotomy MODEL Gene Expression Regulation inflammation CELLS business |
Zdroj: | Experimental Dermatology, 24(8), 623-629. Wiley-Blackwell Experimental dermatology, 24(8), 623-629. Wiley-Blackwell Experimental dermatology, 24(8), 623-629. Blackwell Publishing Ltd van den Broek, L J, van der Veer, W M, de Jong, E H, Gibbs, S & Niessen, F B 2015, ' Suppressed inflammatory gene expression during human hypertrophic scar compared to normotrophic scar formation ', Experimental Dermatology, vol. 24, no. 8, pp. 623-629 . https://doi.org/10.1111/exd.12739 |
ISSN: | 0906-6705 |
DOI: | 10.1111/exd.12739 |
Popis: | Hypertrophic scar formation is a result of adverse cutaneous wound healing. The pathogenesis of hypertrophic scar formation is still poorly understood. A problem next to the lack of suitable animal models is that often normal skin is compared to hypertrophic scar (HTscar) and not to normotrophic scar (NTscar) tissue. Another drawback is that often only one time period after wounding is studied, while scar formation is a dynamic process over a period of several months. In this study, we compared the expression of genes involved in inflammation, angiogenesis and extracellular matrix (ECM) formation and also macrophage infiltration in biopsies obtained before and up to 52weeks after standard surgery in five patients who developed HTscar and six patients who developed NTscar. It was found that HTscar formation coincided with a prolonged decreased expression of inflammatory genes (TNF, IL-1, IL-1RN, CCL2, CCL3, CXCL2, CXCR2, C3 and IL-10) and an extended increased expression of ECM-related genes (PLAU, Col3A1, TGF3). This coincided with a delayed but prolonged infiltration of macrophages (type 2) in HTscar tissue compared to NTscar tissue. These findings were supported by immunohistochemical localization of proteins coding for select genes named above. Our study emphasizes that human cutaneous wound healing is a dynamic process that is needed to be studied over a period of time rather than a single point of time. Taken together, our results suggest innate immune stimulatory therapies may be a better option for improving scar quality than the currently used anti-inflammatory scar therapies. |
Databáze: | OpenAIRE |
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