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Abstract
Chronic non-healing wounds are a major complication of diabetes. Effective communication between immune cells and the extracellular matrix (ECM) is crucial for regulating wound healing. Tumor necrosis factor-stimulated gene-6 (TSG-6) modifies the extracellular matrix (ECM) and regulates inflammation; Thrombospondin 1 (TSP-1) regulates angiogenesis and binds to TSG-6. In both TSG-6 and TSP-1 knockout mice, wound closure is delayed. We hypothesize that hyperglycemia causes dysregulation of TSG-6 and TSP-1, which together results in fewer heavy chain-hyaluronan complexes (HC-HA) in the ECM, an acceleration of leukocyte infiltration, a pro-inflammatory milieu, and wound healing delay.
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