Abstract
In this issue of Blood , Ishihara et al report an entirely novel role for von Willebrand factor (VWF) in promoting wound healing. 1 In particular, they demonstrate that the heparin-binding domain (HBD) within the A1 domain of VWF can bind to a variety of different growth factors, including vascular endothelial growth factor-A (VEGF-A) and platelet-derived growth factor-BB (PDGF-BB). Following a dermal skin injury, delayed wound healing, accompanied by reduced local growth factor concentrations and impaired local angiogenesis, was observed in VWF −/− mice compared with controls (see figure). In contrast, treatment of skin wounds with fibrin matrices functionalized with VWF HBD complexed with VEGF-A and PDGF-BB resulted in improved wound healing in both VWF −/− mice and type 2 diabetic mice. Collectively, these exciting findings suggest that VWF plays a critical role in recruiting growth factors to sites of injury and thereby in regulating tissue repair.
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