ラット骨髄間質細胞においてP2Y2受容体活性化により発生するCa²⁺オシレーションの機構

抄録

Rat bone marrow stromal cells express G protein-coupled purinergic receptor (P2Y₂ receptor). We have investigated intracellular Ca²⁺ signals in these cells using fura-2 AM and found that UTP, an agonist of P2Y₂ receptor, induced not only Ca²⁺ rise but also Ca²⁺ oscillation. Removal of extracellular Ca²⁺ diminished UTP-induced Ca²⁺ oscillation. This fact indicates that the Ca²⁺ oscillation involves Ca²⁺ entry from extracellular space. SKF96365, a blocker for store-operated Ca²⁺ entry channel suppressed UTP-induced Ca²⁺ oscillation. Carbenoxolone (CBX), a gap junction blocker, also suppressed Ca²⁺ oscillation at higher concentration than 50μM, but enhanced at 10μM in some cells. At 10μM, CBX enhanced the peak amplitude of UTP-induced Ca²⁺ rise and kept high Ca²⁺ concentration until CBX was washed out. L-type voltage-dependent Ca²⁺ channel blockers, nifedipine or verapamil did not affect UTP-induced Ca²⁺ oscillation. These results suggest that UTP-induced Ca²⁺ oscillation may be regulated by a complex mechanism including Ca²⁺ entry through store-operated Ca²⁺ channel at plasma membrane and Ca²⁺-transport system via gap junction. [J Physiol Sci. 2006;56 Suppl:S155]