ArticleThrombosis research2012
Modulation of the von Willebrand factor-dependent platelet adhesion through alternative proteolytic pathways.
Article in Thrombosis research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- Plasmin-mediated proteolysis of von Willebrand factor in patients with acute and chronic liver disease.Research and practice in thrombosis and haemostasis · 2025Article
- The Role of HSP47 in Thrombotic Disorders: Molecular Mechanism and Therapeutic Potential.Current issues in molecular biology · 2025Review
- The thrombin generation capability of the Chacma baboon (Papio ursinus): implications for haemostatic disease models.Scientific reports · 2023Article
- Structural hierarchy of mechanical extensibility in human von Willebrand factor multimers.Protein science : a publication of the Protein Society · 2023Article
- The Vascular Endothelium and Coagulation: Homeostasis, Disease, and Treatment, with a Focus on the Von Willebrand Factor and Factors VIII and V.International journal of molecular sciences · 2022Review
- Hemostasis components in cerebral amyloid angiopathy and Alzheimer's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Review
- Acquired von Willebrand Syndrome in Patients With Ventricular Assist Device.Frontiers in medicine · 2019Review
- Effects of Plasmin on von Willebrand Factor and Platelets: A Narrative Review.TH open : companion journal to thrombosis and haemostasis · 2018Review
- Functional cyclophilin D moderates platelet adhesion, but enhances the lytic resistance of fibrin.Scientific reports · 2018Article
- Article
- Review
- Neutrophil Protease Cleavage of Von Willebrand Factor in Glomeruli - An Anti-thrombotic Mechanism in the Kidney.EBioMedicine · 2017Article
- Thrombotic Thrombocytopenic Purpura in Black People: Impact of Ethnicity on Survival and Genetic Risk Factors.PloS one · 2016Article
- ADAMTS13 Secretion and Residual Activity among Patients with Congenital Thrombotic Thrombocytopenic Purpura with and without Renal Impairment.Clinical journal of the American Society of Nephrology : CJASN · 2015Article
- Degradation of platelet-von Willebrand factor complexes by plasmin: an alternative/backup mechanism to ADAMTS13.Circulation · 2014Article
- Proteolytic processing of von Willebrand factor by adamts13 and leukocyte proteases.Mediterranean journal of hematology and infectious diseases · 2013Review
- Modulation of neutrophil (dys)function by Ayurvedic herbs and its potential influence on SARS-CoV-2 infection.Journal of Ayurveda and integrative medicineReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
introductionPlatelet adhesion to collagen under high shear rates depends on the optimal size of the von Willebrand factor (VWF) multimers, which is determined by their limited proteolysis. The present study attempts to identify the role of hemostatic-fibrinolytic enzymes (thrombin, plasmin) and leukocyte-derived proteases (matrix metalloproteinase (MMP)-8, MMP-9, neutrophil elastase) in the cleavage of VWF and to characterize the effect of flow and platelets on this proteolysis and its functional consequences on platelet adhesion. Methods and results According to VWF immunoblots, plasmin, neutrophil elastase and thrombin at concentrations of in vivo relevance resulted in extensive degradation of VWF within several minutes. Platelets protected VWF against this proteolysis under static conditions, whereas perfusion of the proteases at 3350s(-1) shear rate over VWF immobilized on artery cross sections enhanced its degradation and blocked the protective effect of platelets. In parallel with VWF digestion, the examined proteases impaired the VWF-dependent platelet adhesion as reflected in the decreased surface-bound GpIIb/IIIa immunoreactivity following perfusion of collagen-coated surfaces or artery sections with blood and plasmin, neutrophil elastase or thrombin. Within the time frame of minutes no VWF cleavage could be detected under static or flow conditions after exposure to MMP-8 and MMP-9 at concentrations relevant to physiological neutrophil counts.
conclusionOur results indicate a shear- and platelet-dependent role for several proteases in the local modulation of the VWF function.
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Registered trials
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