The effect of arachidonic acid (AA) on intracellular Ca2+ concentration ([Ca2+]i) in human osteoblasts MG63 was studied. AA caused a concentration-dependent increase in [Ca2+]i, mainly due to inward Ca2+ transport from extracellular environment. Moreover, AA in Ca2+ -free medium produced a small, transient increase of [Ca2+]i, indicating that AA may also trigger Ca2+ release from intracellular stores. Because the [Ca2+]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 [Ca2+]i, which, however, was far lower than that obtained with AA. The [Ca2+]i response to AA was not inhibited by nifedipine, suggesting that AA did not activate a voltage-dependent Ca2+ channel. Our results indicate that AA could modulate [Ca2+]i in MG63 human osteoblasts, where it may influence Ca2+ transport across both plasma and endoplasmic membranes. Furthermore, they suggest that osteoblast activity may be modulated by AA.
|Number of pages||6|
|Journal||Prostaglandins Leukotrienes and Essential Fatty Acids|
|Publication status||Published - 1 Aug 2006|
ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology