Related Experiment Videos
Platelet aggregation induced by type IIb platelet von Willebrand factor
H R Gralnick1, L P McKeown, S Williams
1Clinical Pathology Department, National Institutes of Health, Bethesda, MD 20892.
British Journal of Haematology
|February 1, 1989
Summary
Platelet lysates from type IIb von Willebrand's disease (vWd) patients spontaneously aggregate normal platelets. This aggregation is mediated by platelet von Willebrand factor (vWf), not plasma vWf, and is inhibited by specific peptides.
Area of Science:
- Hematology
- Molecular Biology
- Biochemistry
Background:
- Type IIb von Willebrand's disease (vWd) is characterized by spontaneous platelet aggregation and thrombocytopenia.
- The role of platelet-derived von Willebrand factor (vWf) in this process is not fully understood.
Purpose of the Study:
- To investigate the mechanism by which platelet lysates from type IIb vWd patients induce platelet aggregation.
- To differentiate the role of platelet vWf from plasma vWf in aggregation.
Main Methods:
- Incubation of normal and various vWd platelet-rich plasma (PRP) with platelet lysates.
- Use of polyclonal and monoclonal antibodies targeting vWf and its binding domains.
- Testing aggregation with normal platelets in afibrinogenaemic plasma.
- Employing RGDS peptides and fibrinogen gamma chain peptides.
Main Results:
- Type IIb vWd platelet lysates induced aggregation of normal and other vWd PRP, unlike lysates from normal or type I/IIa vWd.
- Aggregation was inhibited by antibodies against plasma vWf but not by those against the GPIb binding domain.
- Aggregation was not dependent on fibrinogen or GPIIb/IIIa interactions.
- Bernard-Soulier PRP aggregated, but Glanzmann's thrombasthenic platelets did not.
- RGDS and fibrinogen gamma chain peptides inhibited aggregation.
Conclusions:
- Platelet-derived vWf in type IIb vWd can directly cause platelet aggregation without added agonists.
- This platelet-mediated aggregation mechanism differs from plasma vWf-mediated interactions in vWd.