In:
European Journal of Endocrinology, Oxford University Press (OUP), Vol. 131, No. 5 ( 1994-11), p. 510-515
Kurzfassung:
Kozawa O, Tokuda H, Suzuki A, Kotoyori J, Ito Y, Oiso Y. Effect of glucocorticoid on prostaglandin F 2α -induced prostaglandin E 2 synthesis in osteoblast-like cells: inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2. Eur J Endocrinol 1994;131:510–15. ISSN 0804–4643 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 PGE 2 , a potent bone resorbing agent, and that the activation of protein kinase C amplifies the PGF 2α -induced PGE 2 synthesis through the potentiation of phospholipase A 2 activity in osteoblast-like MC3T3-E1 cells. In the present study, we examined the effect of dexamethasone on PGE 2 synthesis induced by PGF 2α in MC3T3-E1 cells. The pretreatment with dexamethasone significantly inhibited the PGE 2 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 PGE 2 synthesis induced by melittin, known as a phospholipase A 2 activator. Furthermore, dexamethasone significantly inhibited the enhancement of PGF 2α - or melittin-induced PGE 2 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 PGE 2 synthesis through the inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A 2 in osteoblast-like cells. Osamu Kozawa, Department of Biochemistry, Institute for Developmental Research, Aichi Prefectural Colony, Kasugai, Aichi 480-03, Japan
Materialart:
Online-Ressource
ISSN:
0804-4643
,
1479-683X
DOI:
10.1530/eje.0.1310510
Sprache:
Unbekannt
Verlag:
Oxford University Press (OUP)
Publikationsdatum:
1994
ZDB Id:
1485160-X
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