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Effect of prostaglandin E 2 on phospholipase D activity in osteoblast‐like MC3T3‐E1 cells
Author(s) -
Oiso Yutaka,
Suzuki Atsushi,
Kozawa Osamu
Publication year - 1995
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650100807
Subject(s) - phospholipase d , protein kinase c , pertussis toxin , activator (genetics) , phosphatidic acid , prostaglandin e2 , extracellular , microbiology and biotechnology , chemistry , signal transduction , phospholipase c , g protein , biology , biochemistry , endocrinology , receptor , phospholipid , membrane
Recent evidence indicates that phosphatidylcholine breakdown by phospholipase D (PLD) is an important cellular control mechanism. We investigated the signaling pathway participating in prostaglandin E 2 (PGE 2 )–induced PLD activation in osteoblast‐like MC3T3‐E1 cells. PGE 2 stimulated PLD activity, as measured by choline generated from phosphatidylcholine, just after the stimulation. The reaction reached a plateau 15 minutes later. PGE 2 stimulated PLD activity in a dose‐related manner and also increased inositol phosphate (IP) formation. However, the EC 50 value for PGE 2 ‐induced IP formation is lower than that for PLD activation. 12‐ O ‐Tetradecanoylphorbol‐13‐acetate (TPA), a protein kinase C (PKC) activator, stimulated PLD activity, and a combination of PGE 2 and TPA potentiated it in an additive manner. Although NaF, a heterotrimeric GTP‐binding protein activator, significantly stimulated PLD activity, this effect was not augmented by combination with PGE 2 . PGE 2 ‐induced PLD activity was markedly suppressed by either chelating extracellular Ca 2+ by EGTA or pertussis toxin. These findings suggest that osteoblasts might have at least two PLD activation mechanisms which involve PKC‐dependent or ‐independent pathways. However, present results indicate that PKC is unlikely to be essential to PGE 2 ‐induced PLD activation. On the contrary, pertussis toxin‐sensitive GTP‐binding protein and extracellular Ca 2+ might play important roles in the pathway of PGE 2 ‐induced PLD activation.