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Updated: Oct 1, 2026

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
10:08

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

Involvement of adenosine A2 receptors in the changes of tissue factor-dependent coagulant activity induced by

Tohru Watanabe1, Shogo Tokuyama, Masako Yasuda

  • 1Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan.

Japanese Journal of Pharmacology
|June 6, 2002
PubMed

Insights

Adenosine receptors, specifically the A2 subtype, reduce tissue factor activity and polymorphonuclear leukocyte adhesion to endothelial cells. This suggests a key role for adenosine A2 receptors in regulating these inflammatory and coagulation processes.

Area of Science:

  • Immunology
  • Vascular Biology
  • Pharmacology

Background:

  • Polymorphonuclear leukocytes (PMNs) increase tissue factor (TF) activity in endothelial cells via adhesion.
  • The precise mechanisms regulating PMN-endothelial cell interactions and TF activity are not fully understood.

Purpose of the Study:

  • To investigate the role of adenosine receptors in modulating TF activity and PMN-endothelial cell adhesion.
  • To elucidate the specific adenosine receptor subtypes involved in these processes.

Main Methods:

  • Experiments involved pretreating endothelial cells with adenosine and its receptor agonists/antagonists.
  • Assays measured TF activity and the degree of PMN adhesion to endothelial cells.
  • Specific adenosine receptor agonists (CGS-21680, CPCA) and antagonists (DMPX, CPDMX) were utilized.

Main Results:

  • Adenosine, CGS-21680 (A1/A2 agonist), and CPCA (A2 agonist) significantly reduced TF activity and PMN adhesion in a dose-dependent manner.
  • The adenosine A2-receptor antagonist DMPX reversed the inhibitory effects of adenosine on TF activity and adhesion.
  • The adenosine A1-receptor antagonist CPDMX and A1 agonists (CHA, CCPA) did not affect TF activity or adhesion.

Conclusions:

  • Adenosine A2 receptors play a critical role in inhibiting PMN adhesion to endothelial cells.
  • Inhibition of PMN adhesion via adenosine A2 receptors leads to a reduction in TF activity.
  • Adenosine A2-receptor-mediated pathways represent a potential therapeutic target for modulating inflammation and coagulation.

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