ArticleJournal of thrombosis and haemostasis : JTH2015
Pathological von Willebrand factor fibers resist tissue plasminogen activator and ADAMTS13 while promoting the contact pathway and shear-induced platelet activation.
Article in Journal of thrombosis and haemostasis : JTH, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Computational fluid dynamics-based risk stratification of modified Blalock-Taussig-Thomas shunt thrombogenicity.The Journal of thoracic and cardiovascular surgery · 2026Article
- von Willebrand Factor fibers formed at pathological high shear provide a scaffold for α-synuclein binding and aggregation.Scientific reports · 2026Article
- Polymer embedding of membrane lungs for histological investigations of intra-device clot formation.Frontiers in cardiovascular medicine · 2026Article
- Arterial human blood flow can be stopped by cables of VWF and platelets without coagulation.Blood advances · 2025Article
- Platelet recruitment kinetics are impacted by von Willebrand factor quality in hemostatic adjuncts.Blood vessels, thrombosis & hemostasis · 2025Article
- Impact of Vascular Geometry on Thrombosis in Pediatric Patients With Modified Blalock-Taussig-Thomas Shunt: A Pilot Study.Journal of the American Heart Association · 2025Article
- Role of von Willebrand factor (VWF), platelets, and aberrant flow in the initiation of venous thrombosis.Science advances · 2025Article
- Clot Accumulation in 3D Microfluidic Bifurcating Microvasculature Network.Micromachines · 2024Article
- Shear Histories Alter Local Shear Effects on Thrombus Nucleation and Growth.Annals of biomedical engineering · 2024Article
- Article
- Location, location, location: Fibrin, cells, and fibrinolytic factors in thrombi.Frontiers in cardiovascular medicine · 2022Review
- Point of care whole blood microfluidics for detecting and managing thrombotic and bleeding risks.Lab on a chip · 2021Review
- The Addition of C-Reactive Protein and von Willebrand Factor to Model for End-Stage Liver Disease-Sodium Improves Prediction of Waitlist Mortality.Hepatology (Baltimore, Md.) · 2021Article
- The von Willebrand Factor Facilitates Model for End-Stage Liver Disease-Independent Risk Stratification on the Waiting List for Liver Transplantation.Hepatology (Baltimore, Md.) · 2020Article
- Occlusive thrombosis in arteries.APL bioengineering · 2019Review
- Accumulations of von Willebrand factor within ECMO oxygenators: Potential indicator of coagulation abnormalities in critically ill patients?Artificial organs · 2019Article
- Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation.American journal of physiology. Heart and circulatory physiology · 2019Article
- von Willebrand factor self-association is regulated by the shear-dependent unfolding of the A2 domain.Blood advances · 2019Article
- Antithrombotic therapy in ventricular assist device (VAD) management: From ancient beliefs to updated evidence. A narrative review.International journal of cardiology. Heart & vasculature · 2018Review
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundUnder severe stenotic conditions, von Willebrand factor (VWF) multimerizes into large insoluble fibers at pathological shear rates.
objectiveEvaluate the mechanics and biology of VWF fibers without the confounding effects of endothelium or collagen.
methodsWithin a micropost-impingement microfluidic device, > 100-μm long VWF fibers multimerized on the post within 10 min using EDTA-treated platelet-free plasma (PFP) perfused at wall shear rates > 5000 s(-1) .
resultsvon Willebrand factor fiber thickness increased to > 10 μm as a result of increasing the shear rate to 10,000 s(-1) . In a stress-strain test, fibrous VWF had an elastic modulus of ~50 MPa. The insoluble VWF fibers were non-amyloid because they rapidly dissolved in trypsin, plasmin or 2% SDS, but were resistant to 50 nm ADAMTS13 or 100 nm tissue plasminogen activator in plasma. Following fiber formation, perfusion of low corn trypsin inhibitor (CTI)-treated (4 μg mL(-1) ), recalcified citrated plasma at 1500 s(-1) caused fibrin formation on the VWF fibers, a result not observed with purified type 1 collagen or a naked micropost. During VWF fiber formation, contact pathway factors accumulated on VWF because the use of EDTA/D-Phe-Pro-Arg chloromethylketone (PPACK)/apixaban/high CTI-treated PFP during VWF fiber formation prevented the subsequent fibrin production from low-CTI, recalcified citrated PFP. VWF fibers displayed FXIIa-immunostaining. When PPACK-inhibited whole blood was perfused over VWF fibers, platelets rolled and arrested on the surface of VWF, but only displayed P-selectin if prevailing shear rates were pathological. Platelet arrest on VWF fibers was blocked with αIIb β3 antagonist GR144053.
conclusionsWe report VWF fiber-contact pathway crosstalk and mechanisms of thrombolytic resistance in hemodynamic settings of myocardial infarction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.