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Related Experiment Videos

Adenosine regulates tissue factor expression on endothelial cells

H Deguchi1, H Takeya, H Urano

  • 1Department of Molecular Pathobiology, Mie University School of Medicine, Tsu-city, Japan.

Thrombosis Research
|August 29, 1998
PubMed
Summary
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Adenosine inhibits tissue factor (TF) expression on endothelial cells, potentially via A2a and A3 receptors. This suggests adenosine may offer anticoagulant benefits, especially in conditions like atherosclerosis.

Area of Science:

  • Vascular Biology
  • Endothelial Cell Function
  • Receptor Pharmacology

Background:

  • Tissue factor (TF) expression on endothelial cells is crucial in thrombosis and inflammation.
  • Adenosine signaling through adenosine receptors (ARs) plays a role in vascular homeostasis.
  • Understanding AR subtypes involved in TF regulation is key for therapeutic targeting.

Purpose of the Study:

  • To investigate the inhibitory effect of adenosine on TNF, thrombin, or PMA-induced TF expression in HUVECs.
  • To elucidate the specific roles of A1, A2a, A2b, and A3 ARs in regulating endothelial TF expression.
  • To determine if adenosine exerts anticoagulant activity via specific ARs.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were treated with agonists and antagonists for specific adenosine receptor (AR) subtypes.

Related Experiment Videos

  • TF expression was measured following stimulation with tumor necrosis factor-alpha (TNF), thrombin, or phorbol 12-myristate 13-acetate (PMA).
  • The effects of selective AR agonists (CGS 21680, APNEA, CCPA) and antagonists (PACPX, DMPX) on TF expression were analyzed.

    • Main Results:

    • Adenosine's inhibitory effect on TF expression was confirmed and counteracted by a non-selective AR antagonist.
    • Selective A2aAR and A3AR agonists (CGS 21680, APNEA) inhibited TF expression induced by TNF, thrombin, or PMA.
    • Selective A1AR agonist (CCPA) and A2AR antagonist (DMPX) enhanced TF expression, while A1AR antagonist (PACPX) inhibited it.
    • Basal TF expression was not altered by any agonist or antagonist alone.

    Conclusions:

    • Stimulation of A2aAR and A3AR down-regulates endothelial cell TF expression induced by inflammatory stimuli.
    • Stimulation of A1AR up-regulates endothelial cell TF expression.
    • Adenosine may exert anticoagulant activity on vascular endothelial cells through A2a and A3 receptors, particularly in ischemic or atherosclerotic conditions.