Anandamide activates human platelets through a pathway independent of the arachidonate cascade

Mauro MacCarrone, Monica Bari, Adriana Menichelli, Domenico Del Principe, Alessandro Finazzi Agrò

Research output: Contribution to journalArticle

Abstract

Anandamide (arachidonoylethanolamide, AnNH) is shown to activate human platelets, a process which was not inhibited by acetylsalicylic acid (aspirin). Unlike AnNH, hydroperoxides generated thereof by lipoxygenase activity, and the congener (13-hydroxy)linoleoylethanolamide, were unable to activate platelets, though they counteracted AnNH-mediated stimulation. On the other hand, palmitoylethanolamide neither activated human platelets nor blocked the AnNH effects. AnNH inactivation by human platelets was afforded by a high-affinity transporter, which was activated by nitric oxide-donors up to 225% of the control. The internalized AnNH could thus be hydrolyzed by a fatty acid amide hydrolase (FAAH), characterized here for the first time. Copyright (C) 1999 Federation of European Biochemical Societies.

Original languageEnglish
Pages (from-to)277-282
Number of pages6
JournalFEBS Letters
Volume447
Issue number2-3
DOIs
Publication statusPublished - Mar 26 1999

Keywords

  • Anandamide
  • Arachidonate
  • Endocannabinoid
  • Lipoxygenase
  • Platelet

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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