• Medientyp: E-Artikel
  • Titel: Umbilical cord derived monocytes and platelet rich plasma for diabetic wound healing
  • Beteiligte: Greene-Roos, Jennifer A; Laughlin, Mary
  • Erschienen: The American Association of Immunologists, 2017
  • Erschienen in: The Journal of Immunology
  • Sprache: Englisch
  • DOI: 10.4049/jimmunol.198.supp.81.27
  • ISSN: 0022-1767; 1550-6606
  • Schlagwörter: Immunology ; Immunology and Allergy
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  • Beschreibung: <jats:title>Abstract</jats:title> <jats:p>Chronic non-healing ulcers are a significant complication present in approximately 15% of diabetic patients. Despite standard clinical treatment including wound dressing, debridement of necrotic tissue, and offloading, 15–27% of patients with diabetic ulcer will require amputation. Deep infection is a risk factor for amputation. Platelet rich plasma (PRP) and stem cells have been tested for potential application to treat diabetic ulcers and have been shown to improve wound healing. Umbilical cord blood provides robust cellular and secreted products with therapeutic potential, but remains yet to be fully exploited as a resource for wound healing strategies. Our initial proof of concept studies indicate that umbilical cord blood derived monocytes and platelet rich plasma enhance wound healing processes measured by in vitro assays. When compared to monocytes or platelet rich plasma alone, monocytes and platelet rich plasma significantly enhanced neovascularization as measured by the matrigel angiogenesis assay. Monocytes and platelet rich plasma enhanced fibroblast migration in a wound scratch assay. Additionally, monocytes and platelet rich plasma enhance proliferation of endothelial cells and fibroblasts. Furthermore, these monocytes have potent antibacterial effects as measured by their ability to phagocytose P. aeruginosa in vitro. Collectively, this in vitro data indicates that this product could heal wounds by a mechanism involving enhancing neovascularization, proliferation, migration, and antibacterial activities, all processes which are dysregulated in diabetic wound healing.</jats:p>
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