Key result
Blood outgrowth endothelial cells from type 1 von Willebrand disease patients showed decreased VWF mRNA levels and defects in processing, storage, and secretion compared to healthy controls.
Case-Control (n=17)
Patient-derived blood outgrowth endothelial cells reveal distinct cellular defects in VWF synthesis, processing, and storage across different types of von Willebrand disease.
Patient-derived BOECs may model type 1 VWD cellular defects; leaves open whether phenotypes predict bleeding severity or inform therapy.
Von Willebrand disease (VWD) is a heterogeneous bleeding disorder caused by decrease or dysfunction of von Willebrand factor (VWF). A wide range of mutations in the VWF gene have been characterized; however, their cellular consequences are still poorly understood. Here we have used a recently developed approach to study the molecular and cellular basis of VWD. We isolated blood outgrowth endothelial cells (BOECs) from peripheral blood of 4 type 1 VWD and 4 type 2 VWD patients and 9 healthy controls. We confirmed the endothelial lineage of BOECs, then measured VWF messenger RNA (mRNA) and protein levels (before and after stimulation) and VWF multimers. Decreased mRNA levels were predictive of plasma VWF levels in type 1 VWD, confirming a defect in VWF synthesis. However, BOECs from this group of patients also showed defects in processing, storage, and/or secretion of VWF. Levels of VWF mRNA and protein were normal in BOECs from 3 type 2 VWD patients, supporting the dysfunctional VWF model. However, 1 type 2M patient showed decreased VWF synthesis and storage, indicating a complex cellular defect. These results demonstrate for the first time that isolation of endothelial cells from VWD patients provides novel insight into cellular mechanisms of the disease.
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Starke et al. (2013) conducted a case-control in von Willebrand disease (n=17). von Willebrand disease vs. Healthy controls was evaluated on VWF mRNA and protein levels, and VWF multimers. Blood outgrowth endothelial cells from type 1 von Willebrand disease patients showed decreased VWF mRNA levels and defects in processing, storage, and secretion compared to healthy controls.
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