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  • P2-purinergic receptors in human breast tumor cells: coupling of intracellularcalcium signaling to anion secretion
    Fležar, Matjaž ; Heisler, S.
    ATP increases intracellular Ca++ (šCa++đi) by activating different P2-purinoreceptors. Because ATP increases Cl- secretion in cystic fibrosis (CF)-affected epithelia, the current study was designed ... to establish the link between these two events. Studies were done in epithelial, human MCF-7 breast tumor cells in which the presence of mRNA transcripts encoding CF transmembrane conductance regulator was initially established. Changes in šCa++đi were measured in single cells by fluorescence microscopy; anion transport was measured by 125I efflux. ATP stimulated concentration-dependent increases in šCa++đi and 125I efflux from MCF-7 cells. The relative order of agonist potency of various selective P2-purinoreceptor agonists in increasing šCa++đi and 125I efflux was: UTP > or = ATP > ADP = AMP; 2-chloro-ATP, 2-methylthio-ATP and AMP-phencyclidine were considerably less potent than ATP.The Ca++ ionophore ionomycin increased both intracellular šCa++đi and 125Isecretion. Exposing cells to the intracellular chelator ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetra-acetic acid (EGTA)-acetoxymethylester decreased (AM) decreased ATP- and ionomycin-stimulated 125I efflux. Extracellular EGTA did not alter the Ca++ response to ATP, but inhibited the response to ionomycin. The chelator inhibited both ATP- and ionomycin-induced 125I secretion. Exposure of cells to nifedipine did not affect the responsiveness of MCF-7 cells to ATP. The anion transport antagonist 4,4'-diisothiocyananatostilbene-2,2'-disulfonic acid partially inhibited ATP- and cationophore-stimulated increases in šCa++đi and 125I secretion. The data suggest that activation of P2 receptors in MCF-7 cells leads to an increase inanion transport as a result of the ability of ATP to increase šCa++đi; moreover, anion channel antagonists may produce their inhibitory effect on 125I secretion, in part, by blocking agonist-induced intracellular Ca++ signaling.
    Vir: The Journal of pharmacology and experimental therapeutics. - ISSN 0022-3565 (Letn. 265, št. 3, 1993, str. 1499-1510)
    Vrsta gradiva - članek, sestavni del
    Leto - 1993
    Jezik - angleški
    COBISS.SI-ID - 19043289

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