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DOI: 10.1055/s-2007-1001710
© Georg Thieme Verlag, Stuttgart · New York
Effect of Retinoic Acid on Prostaglandin F2α-Induced Prostaglandin E2 Synthesis in Osteoblast-Like Cells
Publication History
1994
1994
Publication Date:
14 March 2008 (online)
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Summary
We previously reported that prostaglandin F2α (PGF2α) stimulates phosphoinositide hydrolysis via pertussis toxin-sensitive GTP-binding protein in osteoblast-like MC3T3-E1 cells (Miwa, Tokuda, Tsushita, Kotoyori, Takahashi, Ozaki, Kozawa and Oiso 1990) and that PGF2α stimulates arachidonic acid release and prostaglandin E2 (PGE2) synthesis, and the activation of protein kinase C (PKC) amplifies the effect of PGF2α in MC3T3-E1 cells (Tokuda, Oiso and Kozawa 1992). In the present study, we investigated the effect of retinoic acid (RA), a vitamin A (retinol) metabolite, on PGF2α-induced PGE2 synthesis in MC3T3-E1 cells. The pretreatment with RA, which by itself had little effect on synthesis, significantly inhibited PGE2 synthesis induced by PGF2α in a dose-dependent manner in the range between 1 nM and 0.1 μM. This effect of RA was dependent on the time of pretreatment up to 8 h. In addition, RA inhibited the amplification of PGF2α-induced PGE2 synthesis by 12-O-tetradecanoylphorbol-13-acetate, known to be a PKC activator. However, RA had little effect on PGE2 synthesis induced by melittin, known as a phospholipase A2 activator. Moreover, pertussis toxin had little effect on arachidonic acid release induced by PGF2α. These results strongly suggest that RA inhibits PGE2 synthesis induced by PGF2α in osteoblast-like cells and the inhibitory effect is exerted at the point prior to the activation of phospholipase A2.
Key words
Retinoic Acid - Prostaglandin E2 - Osteoblasts