| 18072286 |
Weng JY, Hsu TT, Sun SH: Functional characterization of P2Y1 versus P2X receptors in RBA-2 astrocytes: elucidate the roles of ATP release and protein kinase C. J Cell Biochem. 2008 May 15;104(2):554-67.
A physiological concentration of extracellular ATP stimulated biphasic Ca (2+) signal, and the Ca (2+) transient was decreased and the Ca (2+) sustain was eliminated immediately after removal of ATP and Ca (2+) in RBA-2 astrocytes. Reintroduction of Ca (2+) induced Ca (2+) sustain. Stimulation of P2Y (1) receptors with 2-methylthioadenosine 5'-diphosphate (2MeSADP) also induced a biphasic Ca (2+) signaling and the Ca (2+) sustains were eliminated using Ca (2+)-free buffer. The 2MeSADP-mediated biphasic Ca (2+) signals were inhibited by phospholipase C (PLC) inhibitor U73122, and completely blocked by P2Y (1) selective antagonist MRS2179 and protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) whereas enhanced by PKC inhibitors GF109203X and Go6979. Inhibition of capacitative Ca (2+) entry (CCE) decreased the Ca (2+)-induced Ca (2+) entry; nevertheless, ATP further enhanced the Ca (2+)-induced Ca (2+) entry in the intracellular Ca (2+) store-emptied and CCE-inhibited cells indicating that ATP stimulated Ca (2+) entry via CCE and ionotropic P2X receptors. Furthermore, the 2MeSADP-induced Ca (2+) sustain was eliminated by apyrase but potentiated by P2X (4) allosteric effector ivermectin (IVM). The agonist ADPbetaS stimulated a lesser P2Y (1)-mediated Ca (2+) signal and caused a two-fold increase in ATP release but that were not affected by IVM whereas inhibited by PMA, PLC inhibitor ET-18-OCH (3) and phospholipase D (PLD) inhibitor D609, and enhanced by removal of intra- or extracellular Ca (2+). Taken together, the P2Y (1)-mediated Ca (2+) sustain was at least in part via P2X receptors activated by the P2Y (1)-induced ATP release, and PKC played a pivotal role in desensitization of P2Y (1) receptors in RBA-2 astrocytes. |
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