Arteriovenous Fistula Obstruction and Expression of Platelet Receptors for Von Willebrand Factor and for Fibrinogen (Glycoproteins GPIb and GPIIb/llla) in Hemodialysis Patients

1996 ◽  
Vol 19 (8) ◽  
pp. 451-454 ◽  
Author(s):  
M. Liani ◽  
F. Salvati ◽  
E. Tresca ◽  
G. Dl Paolo ◽  
L. Vitacolonna ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Von Willebrand Factor ◽  
Hemodialysis Patients ◽  
Platelet Surface ◽  
Surface Receptors ◽  
Platelet Receptors ◽  
Stage Renal Disease ◽  
Von Willebrand ◽  
Willebrand Factor

Platelet surface receptors for von Willebrand factor and for fibrinogen (glycoproteins GPIb and GPIIb/llla) were studied with monoclonal antibodies CD42 and CD41 and cytofluorometry in 31 healthy subjects, 10 hemodialysis patients with no A-V fistula obstruction (patent original fistula), 10 hemodialysis patients with frequent A-V fistula obstruction (more than twice), 12 patients with mild chronic renal failure (creatinine 1.75±0.40 mg/100ml), 11 patients with advanced chronic renal failure (creatinine 5.62±1.22 mg/100ml), and 10 patients with end-stage renal disease (ESRD) treated with peritoneal dialysis. There was a significant increase of platelet surface glycoproteins GPIb and GPIIb/llla in the population of hemodialysis patients with frequent A-V fistula obstruction. The expression of these platelet receptors might be related to the prothrombotic tendency of a group of patients with ESRD, who suffer more occlusive and thrombotic events of the A-V fistula. This group of patients may also have a higher frequency of systemic thrombotic and atherosclerotic complications.

Effects of Dietary Manipulation with Fish Oil on Platelet Receptors for von Willebrand Factor and Fibrinogen in Patients with End-Stage Renal Disease

Nephron ◽  
1995 ◽  
Vol 69 (2) ◽  
pp. 170-170 ◽  
Author(s):  
Mario Liani ◽  
Ettore Tresca ◽  
Giuseppe Nubile ◽  
Filippo Salvati ◽  
Pierre Trolliet ◽  
...  
Keyword(s):  
Renal Disease ◽  
Fish Oil ◽  
Von Willebrand Factor ◽  
End Stage Renal Disease ◽  
Dietary Manipulation ◽  
Platelet Receptors ◽  
Stage Renal Disease ◽  
End Stage ◽  
Von Willebrand ◽  
Willebrand Factor

Correlation between Oxidized Low Density Lipoproteins and von Willebrand Factor in Chronic Renal Failure

1996 ◽  
Vol 76 (05) ◽  
pp. 663-669 ◽  
Author(s):  
Paul Holvoet ◽  
Jan Donck ◽  
Michèle Landeloos ◽  
Els Brouwers ◽  
Kristel Luijtens ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Von Willebrand Factor ◽  
Wide Spectrum ◽  
Endothelial Injury ◽  
Maintenance Hemodialysis ◽  
Apo B ◽  
The Individual ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryAn ELISA specific for a wide spectrum of oxidized apo B-100 in OxLDL was developed and applied to blood samples from 27 control subjects, 20 mild chronic renal failure (MCRF) patients, 21 severe chronic renal failure patients on conservative treatment (SCRF) and 56 severe chronic renal failure patients on maintenance hemodialysis (HEMO). Mean levels of OxLDL were 0.59 mg/dl in controls (95% Cl, 0.52-0.66 mg/dl), and were 2.7-fold (p <0.01), 3.1-fold (p <0.001) and 5.4-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Levels of von Willebrand factor, a marker of endothelial injury, were 100 percent in controls (95% Cl, 90-110 percent), and were 1.5-fold (p = NS), 1.6-fold (p <0.01) and 2.1-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Multiple regression analysis revealed that the extent of renal failure (F = 14; p = 0.0004) accounted for a significant fraction of the variation in OxLDL levels, also after exclusion of patients with evidence of ischemic atherosclerotic disease (F = 21; p = 0.0001). After adjustment for the extent of renal failure, hemodialysis (F = 5.6; p = 0.021) and LDL cholesterol levels (F = 7.1, p = 0.0095) contributed significantly to the variation in OxLDL levels. Whereas the extent of renal failure contributed only marginally to the individual variations in vWF levels (F = 4.1; p = 0.048), these levels correlated significantly with plasma levels of OxLDL (F=26; p=0.0001). In conclusion, atherogenic OxLDL increase progressively during the development of renal failure suggesting that the oxidation of LDL may be associated with endothelial injury and atherogenesis in these patients.

scholarly journals Oxidation shuts down an auto-inhibitory mechanism of von Willebrand factor

2019 ◽  
Author(s):  
Rachel Tsai ◽  
Gianluca Interlandi
Keyword(s):  
Von Willebrand Factor ◽  
Blood Protein ◽  
Platelet Surface ◽  
Surface Receptors ◽  
Inhibitory Function ◽  
Methionine Residues ◽  
A Domains ◽  
Oxidation Of Methionine ◽  
Von Willebrand ◽  
Willebrand Factor

AbstractRecently, the platelet-binding function of the blood protein von Willebrand factor (VWF) has been shown to be activated by oxidizing conditions such as created by inflammation. This observation has been linked to the oxidation of methionine residues in three tandem A domains of VWF. Here, we used a dynamic flow assay to investigate which auto-inhibitory mechanisms of VWF are shut down leading to the observed activation. The results show that oxidizing agents do not directly activate the A1 domain, which is the domain in VWF that contains the binding site to platelet surface receptors, but are likely to remove the inhibitory function of neighboring domains of A1.

scholarly journals Factor VIII/von Willebrand factor binding to von Willebrand's disease platelets

Blood ◽  
1982 ◽  
Vol 60 (2) ◽  
pp. 328-332 ◽  
Author(s):  
HR Gralnick ◽  
SB Williams ◽  
BC Shafer ◽  
L Corash
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Von Willebrand Factor ◽  
Von Willebrand's Disease ◽  
Platelet Surface ◽  
Platelet Receptors ◽  
Von Willebrand’S Disease ◽  
Binding Data ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract A form of von Willebrand's disease has been described with enhanced ristocetin-induced platelet aggregation and anodal migration of the factor VIII/von Willebrand factor protein (type IIb). We studied two families with this form of von Willebrand's disease and macrothrombocytopenia. We have found that these platelets bind more of the normal and intermediate-sized multimers of the factor VIII/von Willebrand factor than normal platelets. Analysis of the binding data show an increased affinity of these vWd platelets for the factor VIII/von Willebrand factor. These findings are consistent with an increased number of platelet receptors, which, either by their native topography or migration on the platelet surface, bind factor VIII/von Willebrand factor protein with greater affinity than normal platelets, platelets of other vWd patients, and large platelets of other etiologies.

scholarly journals Factor VIII/von Willebrand factor binding to von Willebrand's disease platelets

Blood ◽  
1982 ◽  
Vol 60 (2) ◽  
pp. 328-332
Author(s):  
HR Gralnick ◽  
SB Williams ◽  
BC Shafer ◽  
L Corash
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Von Willebrand Factor ◽  
Von Willebrand's Disease ◽  
Platelet Surface ◽  
Platelet Receptors ◽  
Von Willebrand’S Disease ◽  
Binding Data ◽  
Von Willebrand ◽  
Willebrand Factor

A form of von Willebrand's disease has been described with enhanced ristocetin-induced platelet aggregation and anodal migration of the factor VIII/von Willebrand factor protein (type IIb). We studied two families with this form of von Willebrand's disease and macrothrombocytopenia. We have found that these platelets bind more of the normal and intermediate-sized multimers of the factor VIII/von Willebrand factor than normal platelets. Analysis of the binding data show an increased affinity of these vWd platelets for the factor VIII/von Willebrand factor. These findings are consistent with an increased number of platelet receptors, which, either by their native topography or migration on the platelet surface, bind factor VIII/von Willebrand factor protein with greater affinity than normal platelets, platelets of other vWd patients, and large platelets of other etiologies.

A Study of Bleeding Time and Von Willebrand Factor in Patients with Chronic Renal Failure

1990 ◽  
Vol 79 (s23) ◽  
pp. 11P-11P
Author(s):  
GTM Robinson ◽  
LR Bond ◽  
S Talbot ◽  
A Chietole ◽  
DH Sevan ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Von Willebrand Factor ◽  
Bleeding Time ◽  
Von Willebrand ◽  
Willebrand Factor

scholarly journals Effect of aspirin on platelet-von Willebrand factor surface expression on thrombin and ADP-stimulated platelets

Blood ◽  
1989 ◽  
Vol 74 (6) ◽  
pp. 2016-2021 ◽  
Author(s):  
RI Parker ◽  
HR Gralnick
Keyword(s):  
Von Willebrand Factor ◽  
Shape Change ◽  
Adenosine Diphosphate ◽  
Surface Expression ◽  
Platelet Surface ◽  
Granule Secretion ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Platelet Shape ◽  
Stimulation Of

Abstract Platelets contain a pool of endogenous platelet-von Willebrand factor (vWF) that becomes expressed on the platelet surface when platelets are stimulated by a variety of agonists. Maximal platelet-vWF expression occurs in concert with platelet alpha-granule secretion. Aspirin (ASA) is known to impair platelet activation and alpha-granule secretion by irreversible inhibition of platelet cyclo-oxygenase. We studied native and ASA-treated platelets for their ability to mobilize and to express platelet-vWF in response to adenosine diphosphate (ADP) or thrombin. We found that each agonist was effective in promoting increased platelet- vWF surface expression on native and ASA-treated platelets. ASA-treated platelets responded identically to native platelets to low (0.01 U/mL) and high (1.0 U/mL) concentrations of thrombin, while the ADP-induced increase in ASA-treated platelets was only 50% to 60% of that for control platelets. Measurement of secreted platelet-vWF and beta- thromboglobulin indicated that the increase seen with ADP was largely independent of alpha-granule secretion. Using monoclonal antibodies (MoAbs) against the platelet glycoproteins (GP) IIb/IIIa and Ib (MoAbs 10E5 and 6D1, respectively), we demonstrated that the ADP-induced increase in platelet-vWF expression on control platelets primarily involved the binding of secreted platelet-vWF to the platelet GPIIb/IIIa. In contrast, the increase in platelet-vWF that occurred following ADP stimulation of ASA-treated platelets was largely insensitive to GPIIb/IIIa blockade. No effect of GPIb blockade in platelet-vWf expression was noted for either control or ASA-treated platelets. When platelet shape change was prevented by the addition of cytochalasin D, ADP-induced platelet-vWf surface expression on ASA- treated platelets was reduced by more than 80%. Our data indicate that platelets in which the cyclooxygenase pathway is blocked by the action of aspirin can increase surface expression of platelet-vWf as a consequence of platelet shape change. We speculate that this process exposes platelet-vWf bound to GPIIb/IIIa, or possibly GPIb, within the surface connected canalicular system.

Adenovirus-induced thrombocytopenia: the role of von Willebrand factor and P-selectin in mediating accelerated platelet clearance

Blood ◽  
2006 ◽  
Vol 109 (7) ◽  
pp. 2832-2839 ◽  
Author(s):  
Maha Othman ◽  
Andrea Labelle ◽  
Ian Mazzetti ◽  
Hisham S. Elbatarny ◽  
David Lillicrap
Keyword(s):  
Von Willebrand Factor ◽  
Cell Activation ◽  
Endothelial Cell Activation ◽  
Platelet Surface ◽  
Adenoviral Gene Transfer ◽  
Coxsackie Adenovirus Receptor ◽  
Transfer Vectors ◽  
Adenovirus Receptor ◽  
Von Willebrand ◽  
Willebrand Factor

AbstractThrombocytopenia has been consistently reported following the administration of adenoviral gene transfer vectors. The mechanism underlying this phenomenon is currently unknown. In this study, we have assessed the influence of von Willebrand Factor (VWF) and P-selectin on the clearance of platelets following adenovirus administration. In mice, thrombocytopenia occurs between 5 and 24 hours after adenovirus delivery. The virus activates platelets and induces platelet-leukocyte aggregate formation. There is an associated increase in platelet and leukocyte-derived microparticles. Adenovirus-induced endothelial cell activation was shown by VCAM-1 expression on virus-treated, cultured endothelial cells and by the release of ultra-large molecular weight multimers of VWF within 1 to 2 hours of virus administration with an accompanying elevation of endothelial microparticles. In contrast, VWF knockout (KO) mice did not show significant thrombocytopenia after adenovirus administration. We have also shown that adenovirus interferes with adhesion of platelets to a fibronectin-coated surface and flow cytometry revealed the presence of the Coxsackie adenovirus receptor on the platelet surface. We conclude that VWF and P-selectin are critically involved in a complex platelet-leukocyte-endothelial interplay, resulting in platelet activation and accelerated platelet clearance following adenovirus administration.

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