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.
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