ISSN:
0730-2312
Keywords:
prostaglandin F2α
;
phospholipase D
;
protein kinase C
;
pertussis toxin
;
GTP-binding protein
;
osteoblast
;
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
Notes:
We previously reported that prostaglandin F2α (PGF2α) receptor is coupled to pertussis toxin (PTX)-sensitive GTP-binding protein (G protein) in osteoblast-like MC3T3-E1 cells [Miwa et al. (1990): Biochem Biophys Res Commun 171:1229-1235]. In the present study, we examined the effect of PGF2α on the activation of phosphatidylcholine-hydrolyzing phospholipase D in MC3T3-E1 cells. PGF2α stimulated the formation of choline in a dose-dependent manner in the range between 10 nM and 10 μM. The formation of choline was stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C (PKC)-activating phorbol ester. 4α-Phorbol 12,13-didecanoate, a PKC-nonactivating phorbol ester, had little effect on choline formation. The formation of choline stimulated by a combination of PGF2α and TPA was additive. Staurosporine, an inhibitor for protein kinases, which inhibited the effect of TPA on choline formation, dose-dependently enhanced the formation of choline induced by PGF2α. NaF, an activator of G protein, stimulated the formation of choline. The formation of choline stimulated by a combination of PGF2α and NaF was not additive. NaF-induced formation of choline was dose-dependently enhanced by staurosporine. PTX dose-dependently inhibited the PGF2α-induced formation of choline. These results strongly suggest that PGF2α activates phospholipase D independently from the activation of PKC in osteoblast-like cells and PTX-sensitive G protein is involved in the PGF2α-induced phospholipase D activation. © 1994 Wiley-Liss, Inc.
Additional Material:
7 Ill.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1002/jcb.240550315
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