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A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
Published on: June 5, 2019
Reduced GPIIb/IIIa expression in platelets hyposensitive to catecholamines when activated with TRAP
Jeong Mi Kim1, Yean Kyoung Koo, Jung Eun Heo
1Natural Products Research Institute, College of Pharmacy, Seoul National University, Seoul 151-742, Korea.
Thrombosis Research
|February 24, 2009
Summary
Platelet aggregation responsiveness to catecholamines (CA) varies in healthy individuals. This study found lower aggregation to other agents and altered glycoprotein expression in CA-hyporesponsive platelets.
Area of Science:
- Hematology
- Platelet Physiology
Background:
- Individual differences in platelet responsiveness to catecholamines (CA) exist in healthy populations.
- Previous studies have categorized individuals into groups based on this variable responsiveness.
Purpose of the Study:
- To investigate the underlying mechanisms contributing to heterogeneous platelet responsiveness to CA in healthy subjects.
- To compare platelet function and surface marker expression between catecholamine-responsive and hyporesponsive individuals.
Main Methods:
- Platelet rich plasma (PRP) aggregation was assessed using turbidimetric methods.
- Platelet glycoprotein and activation marker expression were analyzed via flow cytometry in whole blood.
Main Results:
- Platelets hyporesponsive to CA exhibited significantly lower aggregation responses to arachidonic acid (AA), adenosine diphosphate (ADP), and U46619.
- Flow cytometry revealed higher expression of GPIIb, GPIIIa, and GPIIb/IIIa in the CA-responsive group compared to the hyporesponsive group under TRAP-activated conditions.
- No significant differences in these markers were observed between groups in the resting state.
Conclusions:
- Heterogeneity in catecholamine-induced platelet aggregation is associated with altered platelet function and glycoprotein expression.
- These findings suggest distinct platelet phenotypes contributing to variable responses to agonists in healthy individuals.
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