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A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
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A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets

Marcus E McKenzie1, Alex I Malinin, Christopher R Bell

  • 1Center for Thrombosis Reseasrch, Sinai Hospital of Baltimore, Johns Hopkins University, 2401 West Belvedere Avenue, Baltimore, MD 21215, USA.

Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis
|April 16, 2003
PubMed

Insights

Aspirin directly affects major platelet receptors, beyond blocking prostaglandin synthesis, influencing acute coronary syndrome risk. This study investigated aspirin

Area of Science:

  • Biochemistry
  • Hematology
  • Pharmacology

Background:

  • Aspirin therapy reduces acute coronary syndrome risk via platelet inhibition.
  • The precise mechanisms of aspirin's antiplatelet effects beyond prostaglandin blockade remain unclear.

Purpose of the Study:

  • To investigate the in vitro effects of acetylsalicylic acid (aspirin) on the surface expression of nine key platelet receptors.
  • To elucidate potential non-prostaglandin mediated mechanisms of aspirin's action on platelets.

Main Methods:

  • Whole blood flow cytometry was used to analyze platelet receptor expression in healthy volunteers.
  • Blood samples were treated with varying concentrations of aspirin, with or without apyrase.
  • Surface expression of receptors including GPIIb/IIIa, P-selectin, PECAM-1, and lysosomal-associated membrane proteins was quantified using specific monoclonal antibodies.

Main Results:

  • Aspirin did not affect platelet serotonin release.
  • Dose-dependent inhibition of glycoprotein (GP)IIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed.
  • Apyrase potentiated aspirin's effects and independently inhibited PECAM-1 expression.

Conclusions:

  • Aspirin exerts direct effects on specific platelet receptors, independent of its cyclooxygenase-1 inhibitory action.
  • These findings suggest additional mechanisms contributing to aspirin's antiplatelet efficacy in cardiovascular disease prevention.

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