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Atypical cannabinoid stimulates endothelial cell migration via a Gi/Go-coupled receptor distinct from CB1, CB2 or EDG-1.
Eur J Pharmacol. 2004 Apr 05; 489(1-2):21-7.EJ

Abstract

The endothelium-dependent mesenteric vasorelaxant effect of anandamide has been attributed to stimulation of a Gi/Go-coupled receptor, for which the nonpsychoactive analog abnormal cannabidiol (abn-cbd, (-)-4-(3-3,4-trans-p-menthadien-[1,8]-yl)olivetol) is a selective agonist and the compound O-1918 ((-)-4-(3-3,4-trans-p-menthadien-(1,8)-yl)-orcinol) is a selective antagonist. In human umbilical vein endothelial cells abn-cbd was reported to increase the phosphorylation of p44/42 mitogen activated protein kinase (MAPK) and protein kinase B/Akt, and these effects could be inhibited by pertussis toxin, by phosphatidylinositol 3-kinase (PI3K) inhibitors or by O-1918 [Mol. Pharmacol. 63 (2003) 699]. In the present experiments, abn-cbd caused a concentration-dependent increase in human umbilical vein endothelial cell migration, as quantified in a transwell chamber. This effect was antagonized by O-1918, by the PI3K inhibitor wortmannin, and by pertussis toxin, but not by the cannabinoid CB1 receptor antagonist AM251 or the cannabinoid CB2 receptor antagonist SR144528. The EDG-1 receptor agonist sphingosine-1-phosphate also increased human umbilical vein endothelial cell migration, but this response was unaffected by O-1918. In Chinese hamster ovary cells stably transfected with the gene encoding the EDG-1 receptor, p44/42 MAPK phosphorylation was unaffected by abn-cbd, but strongly induced by sphingosine-1-phosphate. These results indicate that an abn-cbd-sensitive endothelial receptor distinct from cannabinoid CB1, CB2 or EDG-1 receptors mediates not only vasorelaxation but also endothelial cell migration.

Authors+Show Affiliations

Mo FM
Laboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892-8115, USA.
Offertáler L
No affiliation info available
Kunos G
No affiliation info available

MeSH

AndrostadienesAnimalsBlotting, WesternCHO CellsCannabidiolCell MovementCells, CulturedCricetinaeEndothelial CellsEnzyme InhibitorsGTP-Binding Protein alpha Subunits, Gi-GoHumansIndicators and ReagentsLysophospholipidsMitogen-Activated Protein Kinase 1Pertussis ToxinReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Receptors, EstrogenReceptors, G-Protein-CoupledReceptors, LysosphingolipidResorcinolsSphingosineSphingosine-1-Phosphate ReceptorsUmbilical VeinsWortmannin

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15063151

Citation

Mo, Fong Ming, et al. "Atypical Cannabinoid Stimulates Endothelial Cell Migration Via a Gi/Go-coupled Receptor Distinct From CB1, CB2 or EDG-1." European Journal of Pharmacology, vol. 489, no. 1-2, 2004, pp. 21-7.
Mo FM, Offertáler L, Kunos G. Atypical cannabinoid stimulates endothelial cell migration via a Gi/Go-coupled receptor distinct from CB1, CB2 or EDG-1. Eur J Pharmacol. 2004;489(1-2):21-7.
Mo, F. M., Offertáler, L., & Kunos, G. (2004). Atypical cannabinoid stimulates endothelial cell migration via a Gi/Go-coupled receptor distinct from CB1, CB2 or EDG-1. European Journal of Pharmacology, 489(1-2), 21-7.
Mo FM, Offertáler L, Kunos G. Atypical Cannabinoid Stimulates Endothelial Cell Migration Via a Gi/Go-coupled Receptor Distinct From CB1, CB2 or EDG-1. Eur J Pharmacol. 2004 Apr 5;489(1-2):21-7. PubMed PMID: 15063151.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Atypical cannabinoid stimulates endothelial cell migration via a Gi/Go-coupled receptor distinct from CB1, CB2 or EDG-1. AU - Mo,Fong Ming, AU - Offertáler,László, AU - Kunos,George, PY - 2004/02/19/received PY - 2004/02/26/accepted PY - 2004/4/6/pubmed PY - 2004/5/27/medline PY - 2004/4/6/entrez SP - 21 EP - 7 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 489 IS - 1-2 N2 - The endothelium-dependent mesenteric vasorelaxant effect of anandamide has been attributed to stimulation of a Gi/Go-coupled receptor, for which the nonpsychoactive analog abnormal cannabidiol (abn-cbd, (-)-4-(3-3,4-trans-p-menthadien-[1,8]-yl)olivetol) is a selective agonist and the compound O-1918 ((-)-4-(3-3,4-trans-p-menthadien-(1,8)-yl)-orcinol) is a selective antagonist. In human umbilical vein endothelial cells abn-cbd was reported to increase the phosphorylation of p44/42 mitogen activated protein kinase (MAPK) and protein kinase B/Akt, and these effects could be inhibited by pertussis toxin, by phosphatidylinositol 3-kinase (PI3K) inhibitors or by O-1918 [Mol. Pharmacol. 63 (2003) 699]. In the present experiments, abn-cbd caused a concentration-dependent increase in human umbilical vein endothelial cell migration, as quantified in a transwell chamber. This effect was antagonized by O-1918, by the PI3K inhibitor wortmannin, and by pertussis toxin, but not by the cannabinoid CB1 receptor antagonist AM251 or the cannabinoid CB2 receptor antagonist SR144528. The EDG-1 receptor agonist sphingosine-1-phosphate also increased human umbilical vein endothelial cell migration, but this response was unaffected by O-1918. In Chinese hamster ovary cells stably transfected with the gene encoding the EDG-1 receptor, p44/42 MAPK phosphorylation was unaffected by abn-cbd, but strongly induced by sphingosine-1-phosphate. These results indicate that an abn-cbd-sensitive endothelial receptor distinct from cannabinoid CB1, CB2 or EDG-1 receptors mediates not only vasorelaxation but also endothelial cell migration. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/15063151/Atypical_cannabinoid_stimulates_endothelial_cell_migration_via_a_Gi/Go_coupled_receptor_distinct_from_CB1_CB2_or_EDG_1_ DB - PRIME DP - Unbound Medicine ER -