The heparin binding domain of von Willebrand factor binds to growth factors and promotes angiogenesis in wound healing.

ABSTRACT: During wound healing, the distribution, availability, and signaling of growth factors (GFs) are orchestrated by their binding to extracellular matrix components in the wound microenvironment. Extracellular matrix proteins have been shown to modulate angiogenesis and promote wound healing through GF binding. The hemostatic protein von Willebrand factor (VWF) released by endothelial cells (ECs) in plasma and in the subendothelial matrix has been shown to regulate angiogenesis; this function is relevant to patients in whom VWF deficiency or dysfunction is associated with vascular malformations. Here, we show that VWF deficiency in mice causes delayed wound healing accompanied by decreased angiogenesis and decreased amounts of angiogenic GFs in the wound. We show that in vitro VWF binds to sev

SUBMITTER: Ishihara J 

PROVIDER: S-EPMC6566593 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature