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Circulation. 2004 Sep 7;110(10):1326-9. Epub 2004 Jul 12.

gp91phox-dependent expression of platelet CD40 ligand.

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  • 1Divisione IV Clinica Medica, Dipartimento di Medicina Sperimentale e Patologia, Universit√† di Roma La Sapienza, Policlinico Umberto I, 00185, Rome, Italy.

Abstract

BACKGROUND:

CD40 ligand (CD40L) expression on platelets is mediated by agonists, but the underlying mechanism is still unclear.

METHODS AND RESULTS:

CD40L expression was measured in platelets from healthy subjects both with and without the addition of antioxidants or a phospholipase A2 (PLA2) inhibitor and in platelets from 2 patients with an inherited deficiency of gp91phox. Immunoprecipitation analysis was also performed to determine whether normal platelets showed gp91phox expression. Unlike catalase and mannitol, superoxide dismutase inhibited agonist-induced platelet CD40L expression in healthy subjects. Immunoprecipitation analysis also showed that platelets from healthy subjects expressed gp91phox. In 2 male patients with inherited gp91phox deficiency, collagen-, thrombin-, and arachidonic acid-stimulated platelets showed an almost complete absence of superoxide anion (O(2)(-)) and CD40L expression. Incubation of platelets from healthy subjects with a PLA2 inhibitor almost completely prevented agonist-induced O(2)(-) and CD40L expression.

CONCLUSIONS:

These data provide the first evidence that platelet CD40L expression occurs via arachidonic acid-mediated gp91phox activation.

[PubMed - indexed for MEDLINE]
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