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Thromboxane A(2) promotes soluble CD40 ligand release from human platelets.

Yukiko Enomoto¹, Seiji Adachi, Rie Matsushima-Nishiwaki

¹Department of Neurosurgery, Graduate School of Medicine, Gifu University, Gifu, Japan.

Atherosclerosis

|November 26, 2009

Summary

Platelet activation via GPIb/IX/V triggers soluble CD40 ligand (sCD40L) release, mediated by thromboxane A2 (TXA2). This pathway is upregulated in atherosclerosis and responsive to aspirin treatment.

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Area of Science:

Cardiovascular Biology
Platelet Physiology
Inflammation Research

Background:

Soluble CD40 ligand (sCD40L) is elevated in atherosclerosis, promoting inflammation and atherogenesis.
Platelets are key players in thrombotic and inflammatory processes associated with atherosclerosis.

Purpose of the Study:

To investigate the mechanism of sCD40L release from human platelets.
To determine the role of thromboxane A2 (TXA2) in sCD40L release.
To assess the in vivo relevance in patients with carotid artery stenosis.

Main Methods:

In vitro studies using human platelets stimulated with ristocetin to measure sCD40L and TXA2.
Inhibition studies using aspirin, SC-560 (COX-1 inhibitor), ozagrel (TXA2 synthase inhibitor), and a TP antagonist.
In vivo measurements of plasma sCD40L and TXA2 in patients with carotid stenosis and controls.
Assessment of aspirin's effect on plasma markers in patients.

Main Results:

Ristocetin-induced sCD40L release and TXA2 production were significantly correlated in vitro.
Inhibitors of TXA2 synthesis and signaling (aspirin, SC-560, ozagrel, TP antagonist) suppressed sCD40L release.
Plasma sCD40L and TXA2 levels were significantly higher in patients with carotid stenosis compared to controls.
Aspirin treatment markedly reduced plasma TXA2 and sCD40L levels in patients.

Conclusions:

Platelet GPIb/IX/V activation induces sCD40L release through TXA2 generation.
The TXA2-mediated pathway of sCD40L release from platelets is upregulated in atherosclerotic patients.
Targeting the TXA2 pathway, for example with aspirin, may reduce sCD40L levels in atherosclerosis.