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Protein kinase C activation amplifies prostaglandin F 2α ‐induced prostaglandin E 2 synthesis in osteoblast‐like cells
Author(s) -
Tokuda Haruhiko,
Oiso Yutaka,
Kozawa Osamu
Publication year - 1992
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240480306
Subject(s) - protein kinase c , activator (genetics) , arachidonic acid , phospholipase c , chemistry , prostaglandin e2 , phorbol , prostaglandin , prostaglandin e , phospholipase a2 , osteoblast , endocrinology , phospholipase d , medicine , phospholipase , biochemistry , kinase , signal transduction , enzyme , biology , in vitro , receptor
In cloned osteoblast‐like cells, MC3T3‐E1, prostaglandin F 2α (PGF 2α ) stimulated arachidonic acid (AA) release in a dose‐dependent manner in the range between 1 nM and 10 μM. 12‐ O ‐tetradecanoylphorbol‐13‐acetate (TPA), a protein kinase C (PKC) activator, which by itself had little effect on AA release, markedly amplified the release of AA stimulated by PGF 2α in a dose‐dependent manner, 4 α‐phorbol 12, 13‐didecanoate, a phorbol ester which is inactive for PKC, showed little effect on the PGF 2α ‐induced AA release. 1‐oleoyl‐2‐acetylglycerol (OAG), a specific activator for PKC, mimicked TPA by enhancement of the AA release induced by PGF 2α . H‐7, a PKC inhibitor, markedly suppressed the effect of OAG on PGF 2α ‐induced AA release. Quinacrine, a phospholipase A 2 inhibitor, showed partial inhibitory effect on PGF 2α ‐induced AA release, while it suppressed the amplification by OAG of PGF 2α ‐induced AA release almost to the control level. Furthermore, TPA enhanced the AA release induced by melittin, known as a phospholipase A 2 activator. On the other hand, TPA inhibited the formation of inositol triphosphate stimulated by PGF 2α . Under the same condition, PGF 2α indeed stimulated prostaglandin E 2 (PGE 2 ) synthesis and TPA markedly amplified the PGF 2α ‐induced PGE 2 synthesis as well as AA release. These results indicate that the activation of PKC amplifies PGF 2α ‐induced both AA release and PGE 2 synthesis through the potentiation of phospholipase A 2 activity in osteoblast‐like cells.