Abstract
ATP-receptor (P2Y) stimulation induced sustained Ca2+-entry, which was essential for the enhanced cell-proliferation in t-BBEC117, an immortalized cell-line derived from bovine brain endothelial cells. Application of Ca2+ following store-depletion with thapsigargin in Ca2+-free solution induced Ca2+-entry through store-operated channels (SOCs). Ca2+-entry induced by ATP or 1-oleoyl-2-acetyl-sn-glycerol (OAG) together with Ca2+ was significantly larger than that by Ca2+ alone, suggesting the involvement of receptor-operated channels (ROCs) in the Ca2+-entry. Results obtained using pharmacological tools suggest that the contribution of Ca2+ sources to ATP-induced [Ca2+]i rise in t-BBEC117 is estimated as approximately 2:1:2 for Ca2+-release and Ca2+-entry though SOCs and ROCs, respectively.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / pharmacology*
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Animals
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Biological Transport / drug effects
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Blood-Brain Barrier / cytology
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Blood-Brain Barrier / drug effects
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Blood-Brain Barrier / metabolism
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Boron Compounds / pharmacology
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Calcium / metabolism*
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Calcium / pharmacokinetics
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Cattle
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Cell Line, Transformed
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Diglycerides / pharmacology
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Dose-Response Relationship, Drug
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Endothelial Cells / cytology
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Endothelial Cells / drug effects*
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Endothelial Cells / metabolism
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Imidazoles / pharmacology
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Nickel / pharmacology
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TRPC Cation Channels / antagonists & inhibitors
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TRPC Cation Channels / physiology
Substances
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Boron Compounds
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Diglycerides
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Imidazoles
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TRPC Cation Channels
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Nickel
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1-oleoyl-2-acetylglycerol
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Adenosine Triphosphate
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2-aminoethoxydiphenyl borate
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1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole
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Calcium