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The anandamide effect on NO/cGMP pathway in human platelets
Author(s) -
Signorello Maria Grazia,
Giacobbe Enrica,
Passalacqua Mario,
Leoncini Giuliana
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23008
Subject(s) - anandamide , enos , endocannabinoid system , cannabinoid receptor , ly294002 , chemistry , protein kinase b , phosphorylation , pi3k/akt/mtor pathway , nitric oxide , medicine , cannabinoid , endocrinology , pharmacology , microbiology and biotechnology , antagonist , nitric oxide synthase , receptor , signal transduction , biochemistry , biology
In this study the effect of the endocannabinoid anandamide on platelet nitric oxide (NO)/cGMP pathway was investigated. Data report that anandamide in a dose‐and time‐dependent manner increased NO and cGMP levels and stimulated endothelial nitric oxide synthase (eNOS) activity. These parameters were significantly reduced by LY294002, selective inhibitor of PI3K and by MK2206, specific inhibitor of AKT. Moreover anandamide stimulated both eNOSser1177 and AKTser473 phosphorylation. Finally the anandamide effect on NO and cGMP levels, eNOS and AKT phosphorylation/activation were inhibited by SR141716, specific cannabinoid receptor 1 antagonist, supporting the involvement of anandamide binding to this receptor. Overall data of this report indicate that low concentrations of anandamide, through PI3K/AKT pathway activation, stimulates eNOS activity and increases NO levels in human platelets. In such way anandamide contributes to extend platelet survival. J. Cell. Biochem. 112: 924–932, 2011. © 2010 Wiley‐Liss, Inc.