Activation of rabbit blood platelets by anandamide through its cleavage into arachidonic acid

FEBS Letters

Touqui, Lhousseine¹  Mounier, Carine²  Bon, Cassian²  Braud, Sandrine² 

[1] Unité de Pharmacologie Cellulaire/Unité associée INSERM U. 485, Institut Pasteur, Paris, France;Unité des Venins, Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France

关键词: Cannabinoid ligand;    Platelet activation;    Amidase activity;    AA;    arachidonic acid;    PAF;    platelet activating factor;    TxA2;    thromboxane A2;    ANA;    N-arachidonoyl-ethanolamine;    PMSF;    phenylmethylsulfonyl fluoride;   

DOI  :  10.1016/S0014-5793(00)01359-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Anandamide (ANA), a cannabinoid receptor ligand, stimulated platelet aggregation at concentrations similar to those of arachidonic acid (AA). The aggregating effect of ANA was inhibited by aspirin but not by SR-141716, a cannabinoid receptor antagonist. In addition, HU-210, a cannabinoid receptor agonist, failed to induce platelet activation. Radiolabelling experiments showed that exogenous ANA was cleaved by platelets into AA through a phenylmethylsulfonyl fluoride (PMSF)-sensitive pathway. In agreement, PMSF was shown to abolish the aggregating effect of ANA. In conclusion, ANA is able to induce platelet activation via its cleavage by a PMSF-sensitive amidase activity, leading to the release of AA which in turn activates platelets.

【 授权许可】

Unknown