Abstract
The effect of arachidonic acid (AA) on intracellular Ca 2+ concentration ([Ca 2+] i) in human osteoblasts MG63 was studied. AA caused a concentration-dependent increase in [Ca 2+] i, mainly due to inward Ca 2+ transport from extracellular environment. Moreover, AA in Ca 2+ -free medium produced a small, transient increase of [Ca 2+] i, indicating that AA may also trigger Ca 2+ release from intracellular stores. Because the [Ca 2+] i response to AA was inhibited by the cyclooxygenase (COX) inhibitor indomethacin, we tested the effect of prostaglandins (PGs), products of COX pathway. PGs E1 and E2 caused an increase in [Ca 2+] i, which, however, was far lower than that obtained with AA. The [Ca 2+] i response to AA was not inhibited by nifedipine, suggesting that AA did not activate a voltage-dependent Ca 2+ channel. Our results indicate that AA could modulate [Ca 2+] i in MG63 human osteoblasts, where it may influence Ca 2+ transport across both plasma and endoplasmic membranes. Furthermore, they suggest that osteoblast activity may be modulated by AA.
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