What question did this study set out to answer?

To determine how von Willebrand factor and platelet glycoprotein receptors cooperate to support platelet adhesion to fibrin surfaces in flowing blood.

December 1, 1995BloodOpen Access

On the role of von Willebrand factor in promoting platelet adhesion to fibrin in flowing blood

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Authors

SES. C. EndenburgPapworth Hospital RHRR HantganWake Forest University LLLaya Lindeboom-BlokzijlUtrecht University

Discussion

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Implication

Perfusion study reveals that von Willebrand factor must bind platelet glycoprotein Ib to promote adhesion to fibrin under flow, indicating a sequential mechanism for clot stability.

Key Points

To determine how von Willebrand factor and platelet glycoprotein receptors cooperate to support platelet adhesion to fibrin surfaces in flowing blood.
Perfusion of flowing whole blood over fibrin-coated surfaces in a rectangular chamber under high shear rates.
Binding detection using enzyme-linked immunosorbent assay (ELISA), immunoelectron microscopy, and perfusion with severe von Willebrand's disease blood.
Evaluation of receptor interactions using specific monoclonal antibodies and recombinant vWF mutants with altered GPIb or GPIIb:IIIa binding sites.
Plasma von Willebrand factor failed to bind fibrin directly in the absence of platelets, with interactions only detected via immunoelectron microscopy when platelets were present.
vWF mutants lacking the GPIb-binding site abolished adhesion support, whereas mutating the GPIIb:IIIa binding site had no effect, demonstrating vWF binds selectively to GPIb to mediate fibrin attachment.

Cite This Study

Endenburg et al. (1995) studied this question.

synapsesocial.com/papers/6a7731dad8eb58afc2bdb0eb https://doi.org/10.1182/blood.v86.11.4158.bloodjournal86114158

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December 1, 1995BloodOpen Access

On the role of von Willebrand factor in promoting platelet adhesion to fibrin in flowing blood

View Full Paper

Ask AI

Bookmark

Authors

SES. C. EndenburgPapworth Hospital RHRR HantganWake Forest University LLLaya Lindeboom-BlokzijlUtrecht University

Discussion

Member takes

Implication

Perfusion study reveals that von Willebrand factor must bind platelet glycoprotein Ib to promote adhesion to fibrin under flow, indicating a sequential mechanism for clot stability.

Key Points

To determine how von Willebrand factor and platelet glycoprotein receptors cooperate to support platelet adhesion to fibrin surfaces in flowing blood.
Perfusion of flowing whole blood over fibrin-coated surfaces in a rectangular chamber under high shear rates.
Binding detection using enzyme-linked immunosorbent assay (ELISA), immunoelectron microscopy, and perfusion with severe von Willebrand's disease blood.
Evaluation of receptor interactions using specific monoclonal antibodies and recombinant vWF mutants with altered GPIb or GPIIb:IIIa binding sites.
Plasma von Willebrand factor failed to bind fibrin directly in the absence of platelets, with interactions only detected via immunoelectron microscopy when platelets were present.
vWF mutants lacking the GPIb-binding site abolished adhesion support, whereas mutating the GPIIb:IIIa binding site had no effect, demonstrating vWF binds selectively to GPIb to mediate fibrin attachment.

Cite This Study

Endenburg et al. (1995) studied this question.

synapsesocial.com/papers/6a7731dad8eb58afc2bdb0eb https://doi.org/10.1182/blood.v86.11.4158.bloodjournal86114158

Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

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