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dc.contributor.authorDemuth, D.G.
dc.contributor.authorGkoumassi, E.
dc.contributor.authorDroege, M.J.
dc.contributor.authorDekkers, B.G.J.
dc.contributor.authorEsselink, H.J.
dc.contributor.authorVanree, R.M.
dc.contributor.authorParsons, M.
dc.contributor.authorZaagsma, J.
dc.contributor.authorMolleman, A.
dc.contributor.authorNelemans, S.A.
dc.identifier.citationDemuth , D G , Gkoumassi , E , Droege , M J , Dekkers , B G J , Esselink , H J , Vanree , R M , Parsons , M , Zaagsma , J , Molleman , A & Nelemans , S A 2005 , ' Arachidonic Acid Mediates Non-Capacitative Calcium Entry Evoked by CB1-Cannabinoid Receptor Activation in DDT1MF-2 Smooth Muscle Cells ' , Journal of Cellullar Physiology , vol. 205 , no. 1 , pp. 58-67 .
dc.identifier.otherPURE: 123668
dc.identifier.otherPURE UUID: 1d29496e-5e07-47b6-afda-35f3af1ddf3b
dc.identifier.otherdspace: 2299/2478
dc.identifier.otherScopus: 24344487350
dc.description‘The definitive version is available at '. Copyright Wiley-Liss, Inc. DOI: 10.1002/jcp.20390 [Full text of this article is not available in the UHRA]
dc.description.abstractCannabinoid CB1-receptor stimulation in DDT1 MF-2 smooth muscle cells induces a rise in [Ca2+]i, which is dependent on extracellular Ca2+ and modulated by thapsigargin-sensitive stores, suggesting capacitative Ca2+ entry (CCE), and by MAP kinase. Non-capacitative Ca2+ entry (NCCE) stimulated by arachidonic acid (AA) partly mediates histamine H1-receptor-evoked increases in [Ca2+]i in DDT1 MF-2 cells. In the current study, both Ca2+ entry mechanisms and a possible link between MAP kinase activation and increasing [Ca2+]i were investigated. In the whole-cell patch clamp configuration, the CB-receptor agonist CP 55, 940 evoked a transient, Ca2+-dependent K+ current, which was not blocked by the inhibitors of CCE, 2-APB, and SKF 96365. AA, but not its metabolites, evoked a transient outward current and inhibited the response to CP 55,940 in a concentration-dependent manner. CP 55,940 induced a concentration-dependent release of AA, which was inhibited by the CB1 antagonist SR 141716. The non-selective Ca2+ channel blockers La3+ and Gd3+ inhibited the CP 55,940-induced current at concentrations that had no effect on thapsigargin-evoked CCE. La3+ also inhibited the AA-induced current. CP 55,940-induced AA release was abolished by Gd3+ and by phospholipase A2 inhibition using quinacrine; this compound also inhibited the outward current. The CP 55,940-induced AA release was strongly reduced by the MAP kinase inhibitor PD 98059. The data suggest that in DDT1 MF-2 cells, AA is an integral component of the CB1 receptor signaling pathway, upstream of NCCE and, via PLA2, downstream of MAP kinase. © 2005 Wiley-Liss, Inc.en
dc.relation.ispartofJournal of Cellullar Physiology
dc.titleArachidonic Acid Mediates Non-Capacitative Calcium Entry Evoked by CB1-Cannabinoid Receptor Activation in DDT1MF-2 Smooth Muscle Cellsen
dc.contributor.institutionDepartment of Human and Environmental Sciences
dc.description.statusPeer reviewed
rioxxterms.typeJournal Article/Review

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