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J. Biol. Chem., Vol. 277, Issue 16, 14221-14226, April 19, 2002
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From the Departments of Lipid oxidation products promote atherosclerosis
and may also affect osteoporosis. We showed previously that oxidized
lipids including 8-isoprostaglandin E2 (isoPGE2) inhibit osteoblastic differentiation of preosteoblasts. Since osteoporosis is mediated both
by decreased osteoblastic bone formation and by increased osteoclastic
bone resorption, we assessed whether oxidized lipids regulate the
osteoclastic potential of marrow hematopoietic cells. Treatment of
marrow-derived preosteoclasts with isoPGE2 enhanced osteoclastic
differentiation as evidenced by increased tartrate-resistant acid
phosphatase (TRAP) activity and multinucleation, which were inhibited
by calcitonin, and increased numbers of resorption pits. The enhanced
osteoclastic differentiation by isoPGE2 was observed whether
preosteoclasts were in coculture with stromal cells or in
monoculture in the presence of receptor-activated NF
8-Isoprostaglandin E2 Enhances Receptor-activated
NF
B Ligand (RANKL)-dependent Osteoclastic Potential
of Marrow Hematopoietic Precursors via the cAMP Pathway*
§,,, and
Medicine and
Physiology, School of Medicine and ¶ Department of Oral
Radiology, School of Dentistry, UCLA,
Los Angeles, California 90095
B ligand (RANKL)
and macrophage colony-stimulating factor. Receptor antagonist studies
suggest that isoPGE2 effects were mediated by prostaglandin receptor
subtypes EP2/DP on preosteoclasts and subtype EP1 and thromboxane
receptors on stromal/osteoblast cells. The enhanced TRAP activity was
also inhibited by cAMP-dependent protein kinase inhibitors,
and isoPGE2 elevated intracellular cAMP levels of preosteoclast
monocultures. Other oxidized lipids also enhanced the TRAP activity of
preosteoclast monocultures. These data suggest that isoPGE2 enhances
osteoclastic differentiation of marrow preosteoclasts and that this
regulation occurs via the cAMP-dependent protein kinase pathway.
*
This work was supported by Grants HL30568 and HL/AR69261
from the National Institutes of Health and by the Cohen and Laubisch Funds.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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