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von Willebrand factor in experimental malaria-associated acute respiratory distress syndrome Institute of Tropical Medicine KU Leuven

Sirima Kraisin, Sebastien Verhenne, Thy, Kimberly Martinod, Claudia Tersteeg, Nele Vandeputte, Hans Deckmyn, Karen Vanhoorelbeke, Philippe E. Van den Steen, Simon F De Meyer, et al.

Background: Malaria-associated acute respiratory distress syndrome (MA-ARDS) is a lethal complication of severe malaria, characterized by marked pulmonary inflammation. Patient studies have suggested a link between von Willebrand factor (VWF) and malaria severity.

Objectives: To investigate the role of VWF in the pathogenesis of experimental MA-ARDS.

Methods: Plasmodium berghei NK65-E (PbNK65) parasites were injected in Vwf+/+ ...

Clumping factor A, von Willebrand factor-binding protein and von Willebrand factor anchor Staphylococcus aureus to the vessel wall Institute of Tropical Medicine KU Leuven

Jean Claes, Laurens Liesenborghs, ME Peetermans, Tiago Rafael Veloso, Dominique Missiakas, Olaf Schneewind, Silvia Mancini, Jose M Entenza, Marc F Hoylaerts, Ruth Heying, et al.

UNLABELLED: Essentials Staphylococcus aureus (S. aureus) binds to endothelium via von Willebrand factor (VWF). Secreted VWF-binding protein (vWbp) mediates S. aureus adhesion to VWF under shear stress. vWbp interacts with VWF and the Sortase A-dependent surface protein Clumping factor A (ClfA). VWF-vWbp-ClfA anchor S. aureus to vascular endothelium under shear stress.

SUMMARY: Objective When establishing endovascular infections, ...

Sleeping Beauty transposon-mediated gene therapy for von Willebrand disease and the role of von Willebrand factor in abdominal aortic aneurysm KU Leuven

Irina Portier
Von Willebrand disease (VWD) is the most common inherited bleeding disorder in man. It is caused by genetic defects in von Willebrand factor (VWF), a blood protein that is crucial for normal hemostasis. VWD type 3 is the most severe form, characterized by a complete absence of VWF protein. Direct administration of VWF/FVIII containing blood products is currently the only treatment option for VWD type 3. This treatment has however only a ...

Adhesion of Staphylococcus aureus to the vessel wall under flow is mediated by von Willebrand factor-binding protein Institute of Tropical Medicine KU Leuven

Jorien Claes, Thomas Vanassche, Marijke Peetermans, Laurens Liesenborghs, Christophe Vandenbriele, Karen Vanhoorelbeke, Dominique Missiakas, Olaf Schneewind, Marc F Hoylaerts, Ruth Heying, et al.

Adhesion of Staphylococcus aureus to blood vessels under shear stress requires von Willebrand factor (VWF). Several bacterial factors have been proposed to interact with VWF, including VWF-binding protein (vWbp), a secreted coagulase that activates the host's prothrombin to generate fibrin. We measured the adhesion of S aureus Newman and a vWbp-deficient mutant (vwb) to VWF, collagen, and activated endothelial cells in a microparallel flow ...

Pseudohemophilia of Erik von Willebrand caused by homozygous one nucleotide deletion in exon 18 of the VW-factor gene University of Antwerp

Alain Gadisseur, Wilfried Schroyens, Jan J. Michiels
The original description of a novel severe bleeding disorder as Hereditary Pseudohemophilia by Erik von Willebrand can currently be labelled as von Willebrand disease (VWD) type 3. VWD type 3 is autosomal recessive caused by homozygous or double heterozygous null mutations in the von Willebrand factor (VWF) gene and typically characterized by prolonged bleeding time and APTT, FVIII: C levels below 2%, undetectable VWF: Ag, VWF: RCo and VWF: CB ...

Key role of glycoprotein Ib/V/IX and von Willebrand factor in platelet activation-dependent fibrin formation at low shear flow KU Leuven

Hans Deckmyn
A microscopic method was developed to study the role of platelets in fibrin formation. Perfusion of adhered platelets with plasma under coagulating conditions at a low shear rate (250(-1)) resulted in the assembly of a star-like fibrin network at the platelet surface. The focal fibrin formation on platelets was preceded by rises in cytosolic Ca2+, morphologic changes, and phosphatidylserine exposure. Fibrin formation was slightly affected by ...

Laboratory diagnosis and molecular basis of mild von Willebrand disease type 1 University of Antwerp

Jan J. Michiels, Alain Gadiseur, Marc Van Der Planken, Wilfried Schroyens, Huub H.D.M. van Vliet
Mild type 1 von Willebrand disease (VWD) is characterized by low to variable penetrance of bleeding, a high (increased) prevalence of blood group O, von Willebrand factor (VWF) values around and above 30% with normal ratios of VWF:ristocetin cofactor activity (RCo)/VWF:antigen (Ag), VWF:collagen binding (CB)/VWF:Ag and factor VIII (FVIII):coagulant activity (C)/VWF:Ag. Within this group of patients, the combination of the C1584 mutation and ...

Towards novel therapeutic strategies in ischemic stroke by targeting von Willebrand factor and promoting fibrinolysis KU Leuven

Frederik Denorme
Ischemic stroke is worldwide the second most common cause of death and the leading cause of permanent disability. In order to improve therapeutic and prophylactic therapy, it is imperative to understand what causes ischemic stroke and how ischemic stroke brain damage progresses. Up until recently, little was known about the thrombi that cause ischemic stroke. Moreover, experimental and clinical data have demonstrated progression of ischemic ...

Endothelial von Willebrand factor promotes blood-brain barrier flexibility and provides protection from hypoxia and seizures in mice KU Leuven

Simon De Meyer
OBJECTIVE: Aberrant blood-brain barrier (BBB) permeability is a hallmark pathology of many central nervous system diseases. von Willebrand factor (VWF) is stored in endothelial Weibel-Palade bodies from where it is released on activation into plasma and basement membrane. The role of VWF in endothelial homeostasis is unclear. The goal of this study was to assess the role of VWF in disease models associated with increased BBB permeability. ...

Laboratory diagnosis and molecular classification of von Willebrand disease KU Leuven University of Antwerp

Hans Deckmyn
A complete set of laboratory investigations, including bleeding time, PFA-100 closure times, factor VIII (FVIII) coagulant activity (FVIII:C), von Willebrand factor (VWF) ristocetin cofactor (VWF:RCo), collagen binding (VWF:CB), antigen (VWF:Ag) and propeptide (VWFpp), ristocetin-induced platelet aggregation (RIPA), multimeric analysis of VWF and the response of FVIII:C and VWF parameters to desmopressin (DDAVP), is necessary to fully diagnose ...