Effect of retinoic acid on prostaglandin F(2α)-induced phospholipase D activity in osteoblast-like cells

O. Kozawa, Atsushi Suzuki, J. Shinoda, Y. Oiso

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

We previously reported that prostaglandin F(2α) (PGF(2α)) activates phosphatidylcholine-hydrolyzing phospholipase D independently from the activation of protein kinase C (PKC) in osteoblast-like MC3T3-E1 cells, and reported that pertussis toxin-sensitive GTP-binding protein (G-protein) is involved in the PGF(2α)-induced phospholipase D activation. In this study, we examined the effect of retinoic acid (RA) on the phospholipase D activity stimulated by PGF(2α) in these cells. The pretreatment of RA markedly inhibited the formation of choline induced by PGF(2α) (10 μM) in a dose-dependent manner in the range between 1 nM and 0.1 μM. This inhibitory effect of RA was dependent on the time of pretreatment up to 8 h. However, RA had little effect on the choline formation induced by NaF, a G-protein activator, or 12-O-tetradecanoylphorbol-13-acetate, an activator of PKC. These results strongly suggest that RA suppresses the phospholipase D activated by PGF(2α) in osteoblast-like cells and that the effect of RA is exerted at the point between PGF(2α) receptor and G-protein.

Original languageEnglish
Pages (from-to)151-154
Number of pages4
JournalProstaglandins Leukotrienes and Essential Fatty Acids
Volume55
Issue number3
DOIs
Publication statusPublished - 01-01-1996
Externally publishedYes

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Phospholipase D
Osteoblasts
Prostaglandins F
Tretinoin
GTP-Binding Proteins
Choline
Protein Kinase C
Chemical activation
Pertussis Toxin
Tetradecanoylphorbol Acetate
Phosphatidylcholines
Acetates

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Cell Biology

Cite this

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title = "Effect of retinoic acid on prostaglandin F(2α)-induced phospholipase D activity in osteoblast-like cells",
abstract = "We previously reported that prostaglandin F(2α) (PGF(2α)) activates phosphatidylcholine-hydrolyzing phospholipase D independently from the activation of protein kinase C (PKC) in osteoblast-like MC3T3-E1 cells, and reported that pertussis toxin-sensitive GTP-binding protein (G-protein) is involved in the PGF(2α)-induced phospholipase D activation. In this study, we examined the effect of retinoic acid (RA) on the phospholipase D activity stimulated by PGF(2α) in these cells. The pretreatment of RA markedly inhibited the formation of choline induced by PGF(2α) (10 μM) in a dose-dependent manner in the range between 1 nM and 0.1 μM. This inhibitory effect of RA was dependent on the time of pretreatment up to 8 h. However, RA had little effect on the choline formation induced by NaF, a G-protein activator, or 12-O-tetradecanoylphorbol-13-acetate, an activator of PKC. These results strongly suggest that RA suppresses the phospholipase D activated by PGF(2α) in osteoblast-like cells and that the effect of RA is exerted at the point between PGF(2α) receptor and G-protein.",
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Effect of retinoic acid on prostaglandin F(2α)-induced phospholipase D activity in osteoblast-like cells. / Kozawa, O.; Suzuki, Atsushi; Shinoda, J.; Oiso, Y.

In: Prostaglandins Leukotrienes and Essential Fatty Acids, Vol. 55, No. 3, 01.01.1996, p. 151-154.

Research output: Contribution to journalArticle

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T1 - Effect of retinoic acid on prostaglandin F(2α)-induced phospholipase D activity in osteoblast-like cells

AU - Kozawa, O.

AU - Suzuki, Atsushi

AU - Shinoda, J.

AU - Oiso, Y.

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AB - We previously reported that prostaglandin F(2α) (PGF(2α)) activates phosphatidylcholine-hydrolyzing phospholipase D independently from the activation of protein kinase C (PKC) in osteoblast-like MC3T3-E1 cells, and reported that pertussis toxin-sensitive GTP-binding protein (G-protein) is involved in the PGF(2α)-induced phospholipase D activation. In this study, we examined the effect of retinoic acid (RA) on the phospholipase D activity stimulated by PGF(2α) in these cells. The pretreatment of RA markedly inhibited the formation of choline induced by PGF(2α) (10 μM) in a dose-dependent manner in the range between 1 nM and 0.1 μM. This inhibitory effect of RA was dependent on the time of pretreatment up to 8 h. However, RA had little effect on the choline formation induced by NaF, a G-protein activator, or 12-O-tetradecanoylphorbol-13-acetate, an activator of PKC. These results strongly suggest that RA suppresses the phospholipase D activated by PGF(2α) in osteoblast-like cells and that the effect of RA is exerted at the point between PGF(2α) receptor and G-protein.

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