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pubmed:abstractText |
We found that stimulation of P2Y2 receptor (P2Y2R), which is endogenously expressed in CHO-K1 cells, induced intracellular calcium ([Ca2+]i) oscillation with a low frequency of 11.4 +/- 2.7 mHz. When CHO-K1 cells expressing GFP-tagged kinase-negative gammaPKC (gammaPKC-KN-GFP), which is a neuron-specific subtype of PKC, were stimulated with UDP, gammaPKC-KN-GFP, but not wild-type gammaPKC (gammaPKC-GFP) showed an oscillatory translocation. The oscillatory translocation of gammaPKC-KN-GFP corresponded with [Ca2+]i oscillation, which was not observed in the cells expressing gammaPKC-GFP. We examined the mechanism ofP2Y2R-induced [Ca2+]i oscillation pharmacologically. gammaPKC-KN-GFP oscillation was stopped by an extracellular Ca2+ chelator, EGTA, an antagonist of P2Y2R, Suramin, and store-operated calcium channel (SOC) inhibitors, SKF96365 and 2-ABP. Taken together, P2Y2R-induced [Ca2+]i oscillation in CHO-K1 cells is related with Ca2+ influx through SOC, whose function may be negatively regulated by gammaPKC. This [Ca2]i oscillation was distinct from that induced by metabotropic glutamate receptor 5 (mGluR5) stimulation in the frequency (72.3 +/- 5.3 mHz) and in the regulatory mechanism.
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pubmed:affiliation |
Laboratory of Molecular Pharmacology, Biosignal Research Center, Kobe University, Rokkodai-cho 1-1, Nada-ku, Kobe 657-8501, Japan.
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