Effect of glucocorticoid on prostaglandin F(2α)-induced prostaglandin E2 synthesis in osteoblast-like cells

Inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2

O. Kozawa, H. Tokuda, Atsushi Suzuki, J. Kotoyori, Y. Ito, Y. Oiso

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Abstract

It is well known that osteoporosis is a common complication of patients with glucocorticoid excess. We showed previously that prostaglandin (PG) F(2α), stimulates the synthesis of PGE2, a potent bone resorbing agent, and that the activation of protein kinase C amplifies the PGF(2α)-induced PGE2 synthesis through the potentiation of phospholipase A2 activity in osteoblast-like MC3T3-E1 cells. In the present;study, we examined the effect of dexamethasone on PGE2 synthesis induced by PGF(2α), in MC3T3-E1 cells. The pretreatment with dexamethasone significantly inhibited the PGE2 synthesis in a dose-dependent manner in the range between 0.1 and 10 nmol/l in these cells. This effect of dexamethasone was dependent on the time of pretreatment up to 8 h. Dexamethasone also inhibited PGE2 synthesis induced by melittin, known as a phospholipase A2 activator. Furthermore, dexamethasone significantly inhibited the enhancement of PGF(2α)- or melittin-induced PGE2 synthesis by 12-O-tetradecanoylphorbol-13-acetate, known as a protein kinase C activator. In addition, dexamethasone significantly inhibited PGF(2α)-induced formation of inositol phosphates in a dose-dependent manner between 0.1 and 10 nmol/l in MC3T3-E1 cells. These results strongly suggest that glucocorticoid inhibits PGF(2α)-induced PGE2 synthesis through the inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2 in osteoblast-like cells.

Original languageEnglish
Pages (from-to)510-515
Number of pages6
JournalEuropean Journal of Endocrinology
Volume131
Issue number5
DOIs
Publication statusPublished - 01-01-1994
Externally publishedYes

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Phosphoinositide Phospholipase C
Phospholipases A2
Prostaglandins F
Osteoblasts
Dinoprostone
Glucocorticoids
Hydrolysis
Dexamethasone
Melitten
Protein Kinase C
Inositol Phosphates
Tetradecanoylphorbol Acetate
Osteoporosis
Bone and Bones

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

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title = "Effect of glucocorticoid on prostaglandin F(2α)-induced prostaglandin E2 synthesis in osteoblast-like cells: Inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2",
abstract = "It is well known that osteoporosis is a common complication of patients with glucocorticoid excess. We showed previously that prostaglandin (PG) F(2α), stimulates the synthesis of PGE2, a potent bone resorbing agent, and that the activation of protein kinase C amplifies the PGF(2α)-induced PGE2 synthesis through the potentiation of phospholipase A2 activity in osteoblast-like MC3T3-E1 cells. In the present;study, we examined the effect of dexamethasone on PGE2 synthesis induced by PGF(2α), in MC3T3-E1 cells. The pretreatment with dexamethasone significantly inhibited the PGE2 synthesis in a dose-dependent manner in the range between 0.1 and 10 nmol/l in these cells. This effect of dexamethasone was dependent on the time of pretreatment up to 8 h. Dexamethasone also inhibited PGE2 synthesis induced by melittin, known as a phospholipase A2 activator. Furthermore, dexamethasone significantly inhibited the enhancement of PGF(2α)- or melittin-induced PGE2 synthesis by 12-O-tetradecanoylphorbol-13-acetate, known as a protein kinase C activator. In addition, dexamethasone significantly inhibited PGF(2α)-induced formation of inositol phosphates in a dose-dependent manner between 0.1 and 10 nmol/l in MC3T3-E1 cells. These results strongly suggest that glucocorticoid inhibits PGF(2α)-induced PGE2 synthesis through the inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2 in osteoblast-like cells.",
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T2 - Inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2

AU - Kozawa, O.

AU - Tokuda, H.

AU - Suzuki, Atsushi

AU - Kotoyori, J.

AU - Ito, Y.

AU - Oiso, Y.

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N2 - It is well known that osteoporosis is a common complication of patients with glucocorticoid excess. We showed previously that prostaglandin (PG) F(2α), stimulates the synthesis of PGE2, a potent bone resorbing agent, and that the activation of protein kinase C amplifies the PGF(2α)-induced PGE2 synthesis through the potentiation of phospholipase A2 activity in osteoblast-like MC3T3-E1 cells. In the present;study, we examined the effect of dexamethasone on PGE2 synthesis induced by PGF(2α), in MC3T3-E1 cells. The pretreatment with dexamethasone significantly inhibited the PGE2 synthesis in a dose-dependent manner in the range between 0.1 and 10 nmol/l in these cells. This effect of dexamethasone was dependent on the time of pretreatment up to 8 h. Dexamethasone also inhibited PGE2 synthesis induced by melittin, known as a phospholipase A2 activator. Furthermore, dexamethasone significantly inhibited the enhancement of PGF(2α)- or melittin-induced PGE2 synthesis by 12-O-tetradecanoylphorbol-13-acetate, known as a protein kinase C activator. In addition, dexamethasone significantly inhibited PGF(2α)-induced formation of inositol phosphates in a dose-dependent manner between 0.1 and 10 nmol/l in MC3T3-E1 cells. These results strongly suggest that glucocorticoid inhibits PGF(2α)-induced PGE2 synthesis through the inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2 in osteoblast-like cells.

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