We previously reported that prostaglandin F(2α) (PGF(2α)) 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 PGF(2α), stimulates arachidonic acid release and prostaglandin E2 (PGE2) synthesis, and the activation of protein kinase C (PKC) amplifies the effect of PGF(2α), 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 PGF(2α)-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 PGF(2α), 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 PGF(2α)-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 PGF(2α). These results strongly suggest that RA inhibits PGE2 synthesis induced by PGF(2α), in osteoblast-like cells and the inhibitory effect is exerted at the point prior to the activation of phospholipase A2.
|Number of pages||5|
|Journal||Hormone and Metabolic Research|
|Publication status||Published - 01-01-1994|
All Science Journal Classification (ASJC) codes
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical