http://www.cnr.it/ontology/cnr/individuo/prodotto/ID14736

The uptake by cells of 2-arachidonoylglycerol, an endogenous agonist of cannabinoid receptors (Articolo in rivista)

Type

Articolo in rivista (Classe)
Prodotto della ricerca (Classe)

Label

The uptake by cells of 2-arachidonoylglycerol, an endogenous agonist of cannabinoid receptors (Articolo in rivista) (literal)

Anno

2001-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1046/j.1432-1327.2001.02072.x (literal)

Alternative label

Bisogno T., Maccarrone M., De Petrocellis L., Jarrahian A., Finazzi-Agrò A., Hillard C. and Di Marzo V. (2001)
The uptake by cells of 2-arachidonoylglycerol, an endogenous agonist of cannabinoid receptors
in European journal of biochemistry (Print); FEBS, Federation of european biochemical societies, London (Regno Unito)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Bisogno T., Maccarrone M., De Petrocellis L., Jarrahian A., Finazzi-Agrò A., Hillard C. and Di Marzo V. (literal)

Pagina inizio

1982 (literal)

Pagina fine

1989 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

268 (literal)

Rivista

European journal of biochemistry (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

7 (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

1. Ist Chim Mol Interesse Biol, Endocannabinoid Res Grp, I-80072 Arco, Italy 2. CNR, Ist Cibernet, Endocannabinoid Res Grp, I-80125 Naples, Italy 3. Univ Rome Tor Vergata, Dept Expt Med & Biochem Sci, I-00173 Rome, Italy 4. Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA (literal)

Titolo

The uptake by cells of 2-arachidonoylglycerol, an endogenous agonist of cannabinoid receptors (literal)

Abstract

It is not yet clear if the endocannabinoid 2-arachidonoylglycerol (2-AG) is transported into cells through the same membrane transporter mediating the uptake of the other endogenous cannabinoid, anandamide (N-arachidonoylethanolamine, AEA), and whether this process (a) is regulated by cells and (b) limits 2-AG pharmacological actions. We have studied simultaneously the facilitated transport of [14C]AEA and [3H]2-AG into rat C6 glioma cells and found uptake mechanisms with different efficacies but similar affinities for the two compounds (Km 11.0 +/- 2.0 and 15.3 +/- 3.1 microM, Bmax 1.70 +/- 0.30 and 0.24 +/- 0.04 nmol.min-1.mg protein-1, respectively). Despite these similar Km values, 2-AG inhibits [14C]AEA uptake by cells at concentrations (Ki = 30.1 +/- 3.9 microM) significantly higher than those required to either 2-AG or AEA to inhibit [3H]2-AG uptake (Ki = 18.9 +/- 1.8 and 20.5 +/- 3.2 microM, respectively). Furthermore: (a) if C6 cells are incubated simultaneously with identical concentrations of [14C]AEA and [3H]2-AG, only the uptake of the latter compound is significantly decreased as compared to that observed with [3H]2-AG alone; (b) the uptake of [14C]AEA and [3H]2-AG by cells is inhibited with the same potency by AM404 (Ki = 7.5 +/- 0.7 and 10.2 +/- 1.7 microM, respectively) and linvanil (Ki = 9.5 +/- 0.7 and 6.4 +/- 1.2 microM, respectively), two inhibitors of the AEA membrane transporter; (c) nitric oxide (NO) donors enhance the uptake of both [14C]AEA and [3H]2-AG, thus suggesting that 2-AG action can be regulated through NO release; (d) AEA and 2-AG induce a weak release of NO that can be blocked by a CB1 cannabinoid receptor antagonist, and significantly enhanced in the presence of AM404 and linvanil, thus suggesting that transport into C6 cells limits the action of both endocannabinoids. (literal)

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