5-Lipoxygenase metabolites of arachidonic acid stimulate isolated osteoclasts to resorb calcified matrices

Wolf E. Gallwitz, Gregory R. Mundy, Chang H. Lee, Mei Qiao, G. David Roodman, Mark Raftery, Simon J. Gaskell, Lynda Bonewald

Research output: Contribution to journalArticle

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Abstract

Bone resorption requires cooperation between osteoclasts and mononuclear accessory cells by mechanisms which have not been elucidated. Since multinucleated cells in giant cell tumors of bone have many phenotypic and functional characteristics of normal osteoclasts, we have examined the interaction between the boneresorbing multinucleated cells and the distinct mononuclear stromal cells from these tumors. We have found that these mononuclear cells produce an activity which stimulates both giant cells from giant cell tumors and rodent osteoclasts to resorb bone in vitro. We have identified the activity and found that it represents several products of the 5-lipoxygenase pathway of arachidonic acid metabolism, namely 5-hydroxyeicosatetraenoic acid and the Ieukotrienes. These data indicate that 5-lipoxygenase metabolites stimulate isolated osteoclasts to resorb bone in vitro and may represent a mechanism by which mononuclear stromal cells in human giant cell tumors communicate with the giant cells. In addition, these results may explain a possible mechanism for communication between accessory cells and osteoclasts involved in normal bone resorption.

Original languageEnglish (US)
Pages (from-to)10087-10094
Number of pages8
JournalJournal of Biological Chemistry
Volume268
Issue number14
StatePublished - May 15 1993
Externally publishedYes

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Arachidonate 5-Lipoxygenase
Osteoclasts
Metabolites
Arachidonic Acid
Bone
Tumors
Giant Cell Tumors
Accessories
Giant Cells
Bone Resorption
Stromal Cells
Giant Cell Tumor of Bone
Bone and Bones
Metabolism
Rodentia
Communication
Neoplasms

ASJC Scopus subject areas

  • Biochemistry

Cite this

5-Lipoxygenase metabolites of arachidonic acid stimulate isolated osteoclasts to resorb calcified matrices. / Gallwitz, Wolf E.; Mundy, Gregory R.; Lee, Chang H.; Qiao, Mei; Roodman, G. David; Raftery, Mark; Gaskell, Simon J.; Bonewald, Lynda.

In: Journal of Biological Chemistry, Vol. 268, No. 14, 15.05.1993, p. 10087-10094.

Research output: Contribution to journalArticle

Gallwitz, WE, Mundy, GR, Lee, CH, Qiao, M, Roodman, GD, Raftery, M, Gaskell, SJ & Bonewald, L 1993, '5-Lipoxygenase metabolites of arachidonic acid stimulate isolated osteoclasts to resorb calcified matrices', Journal of Biological Chemistry, vol. 268, no. 14, pp. 10087-10094.
Gallwitz, Wolf E. ; Mundy, Gregory R. ; Lee, Chang H. ; Qiao, Mei ; Roodman, G. David ; Raftery, Mark ; Gaskell, Simon J. ; Bonewald, Lynda. / 5-Lipoxygenase metabolites of arachidonic acid stimulate isolated osteoclasts to resorb calcified matrices. In: Journal of Biological Chemistry. 1993 ; Vol. 268, No. 14. pp. 10087-10094.
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AU - Mundy, Gregory R.

AU - Lee, Chang H.

AU - Qiao, Mei

AU - Roodman, G. David

AU - Raftery, Mark

AU - Gaskell, Simon J.

AU - Bonewald, Lynda

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AB - Bone resorption requires cooperation between osteoclasts and mononuclear accessory cells by mechanisms which have not been elucidated. Since multinucleated cells in giant cell tumors of bone have many phenotypic and functional characteristics of normal osteoclasts, we have examined the interaction between the boneresorbing multinucleated cells and the distinct mononuclear stromal cells from these tumors. We have found that these mononuclear cells produce an activity which stimulates both giant cells from giant cell tumors and rodent osteoclasts to resorb bone in vitro. We have identified the activity and found that it represents several products of the 5-lipoxygenase pathway of arachidonic acid metabolism, namely 5-hydroxyeicosatetraenoic acid and the Ieukotrienes. These data indicate that 5-lipoxygenase metabolites stimulate isolated osteoclasts to resorb bone in vitro and may represent a mechanism by which mononuclear stromal cells in human giant cell tumors communicate with the giant cells. In addition, these results may explain a possible mechanism for communication between accessory cells and osteoclasts involved in normal bone resorption.

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