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

Marcus E. McKenzie, Alex I. Malinin, Christopher R. Bell, Alex Dzhanashvili, Eric D. Horowitz, Benjamin R. Oshrine, Dan Atar, Victor L. Serebruany

Research output: Contribution to journalArticle

Abstract

Platelet inhibition after aspirin therapy reduces the risk for the development of acute coronary syndromes. However, the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear. We sought to determine the in vitro effects of aspirin on the surface expression of nine platelet receptors using whole blood flow cytometry. Blood from 24 healthy volunteers was incubated for 30 min with 1.8 and 7.2 mg/l phosphate-buffered saline-diluted acetylsalicylic acid in the presence or absence of apyrase. Platelet serotonin release, and the surface expression of platelet receptors with or without apyrase were determined using the following monoclonal antibodies: anit-CD41 [glycoprotein (GP)IIb/IIIa], CD42b (GPIb), CD62p (P-selectin), CD51/CD61 (vitronectin receptor), CD31 [platelet/endothelial cellular adhesion molecule-1 (PECAM-1)], CD107a [lysosomal associated membrane protein (LAMP)-1], CD107b (LAMP-2), CD63 (LIMP or LAMP-3), and CD151 (PETA-3). Samples were then immediately fixed with 2% paraformaldehyde, and run on the flow cytometer within 48 h. Aspirin does not affect serotonin release from human platelets. Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples. Apyrase potentiates the effects of aspirin, and independently inhibits PECAM-1. In addition to the known effect of irreversibly inhibiting platelet cyclooxygenase-1, thereby blocking thromboxane A2 synthesis, it appears that aspirin exhibits direct effects on selective major platelet receptors.

Original languageEnglish (US)
Pages (from-to)249-253
Number of pages5
JournalBlood Coagulation and Fibrinolysis
Volume14
Issue number3
DOIs
StatePublished - Apr 2003

Fingerprint

Platelet Glycoprotein GPIIb-IIIa Complex
P-Selectin
Membrane Glycoproteins
Aspirin
Blood Platelets
Apyrase
Lysosomal-Associated Membrane Protein 3
Lysosomal-Associated Membrane Protein 2
CD63 Antigen
Lysosomal-Associated Membrane Protein 1
Serotonin
Integrin alphaVbeta3
Cyclooxygenase 1
Thromboxane A2
Acute Coronary Syndrome
Prostaglandins
Healthy Volunteers
Flow Cytometry
Phosphates
Monoclonal Antibodies

Keywords

  • Apyrase
  • Aspirin
  • Flow cytometry
  • Human
  • Platelets
  • Serotonin

ASJC Scopus subject areas

  • Hematology

Cite this

McKenzie, M. E., Malinin, A. I., Bell, C. R., Dzhanashvili, A., Horowitz, E. D., Oshrine, B. R., ... Serebruany, V. L. (2003). Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets. Blood Coagulation and Fibrinolysis, 14(3), 249-253. https://doi.org/10.1097/00001721-200304000-00005

Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets. / McKenzie, Marcus E.; Malinin, Alex I.; Bell, Christopher R.; Dzhanashvili, Alex; Horowitz, Eric D.; Oshrine, Benjamin R.; Atar, Dan; Serebruany, Victor L.

In: Blood Coagulation and Fibrinolysis, Vol. 14, No. 3, 04.2003, p. 249-253.

Research output: Contribution to journalArticle

McKenzie, ME, Malinin, AI, Bell, CR, Dzhanashvili, A, Horowitz, ED, Oshrine, BR, Atar, D & Serebruany, VL 2003, 'Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets', Blood Coagulation and Fibrinolysis, vol. 14, no. 3, pp. 249-253. https://doi.org/10.1097/00001721-200304000-00005
McKenzie, Marcus E. ; Malinin, Alex I. ; Bell, Christopher R. ; Dzhanashvili, Alex ; Horowitz, Eric D. ; Oshrine, Benjamin R. ; Atar, Dan ; Serebruany, Victor L. / Aspirin inhibits surface glycoprotein IIb/IIIa, P-selectin, CD63, and CD107a receptor expression on human platelets. In: Blood Coagulation and Fibrinolysis. 2003 ; Vol. 14, No. 3. pp. 249-253.
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abstract = "Platelet inhibition after aspirin therapy reduces the risk for the development of acute coronary syndromes. However, the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear. We sought to determine the in vitro effects of aspirin on the surface expression of nine platelet receptors using whole blood flow cytometry. Blood from 24 healthy volunteers was incubated for 30 min with 1.8 and 7.2 mg/l phosphate-buffered saline-diluted acetylsalicylic acid in the presence or absence of apyrase. Platelet serotonin release, and the surface expression of platelet receptors with or without apyrase were determined using the following monoclonal antibodies: anit-CD41 [glycoprotein (GP)IIb/IIIa], CD42b (GPIb), CD62p (P-selectin), CD51/CD61 (vitronectin receptor), CD31 [platelet/endothelial cellular adhesion molecule-1 (PECAM-1)], CD107a [lysosomal associated membrane protein (LAMP)-1], CD107b (LAMP-2), CD63 (LIMP or LAMP-3), and CD151 (PETA-3). Samples were then immediately fixed with 2{\%} paraformaldehyde, and run on the flow cytometer within 48 h. Aspirin does not affect serotonin release from human platelets. Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples. Apyrase potentiates the effects of aspirin, and independently inhibits PECAM-1. In addition to the known effect of irreversibly inhibiting platelet cyclooxygenase-1, thereby blocking thromboxane A2 synthesis, it appears that aspirin exhibits direct effects on selective major platelet receptors.",
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AB - Platelet inhibition after aspirin therapy reduces the risk for the development of acute coronary syndromes. However, the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear. We sought to determine the in vitro effects of aspirin on the surface expression of nine platelet receptors using whole blood flow cytometry. Blood from 24 healthy volunteers was incubated for 30 min with 1.8 and 7.2 mg/l phosphate-buffered saline-diluted acetylsalicylic acid in the presence or absence of apyrase. Platelet serotonin release, and the surface expression of platelet receptors with or without apyrase were determined using the following monoclonal antibodies: anit-CD41 [glycoprotein (GP)IIb/IIIa], CD42b (GPIb), CD62p (P-selectin), CD51/CD61 (vitronectin receptor), CD31 [platelet/endothelial cellular adhesion molecule-1 (PECAM-1)], CD107a [lysosomal associated membrane protein (LAMP)-1], CD107b (LAMP-2), CD63 (LIMP or LAMP-3), and CD151 (PETA-3). Samples were then immediately fixed with 2% paraformaldehyde, and run on the flow cytometer within 48 h. Aspirin does not affect serotonin release from human platelets. Dose-dependent inhibition of GPIIb/IIIa, P-selectin, CD63, and CD107a receptor expression was observed in the aspirin-treated whole-blood samples. Apyrase potentiates the effects of aspirin, and independently inhibits PECAM-1. In addition to the known effect of irreversibly inhibiting platelet cyclooxygenase-1, thereby blocking thromboxane A2 synthesis, it appears that aspirin exhibits direct effects on selective major platelet receptors.

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