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Prostaglandin E 2 inhibits formation of osteoclastlike cells in long‐term human marrow cultures but is not a mediator of the inhibitory effects of transforming growth factor β
Author(s) -
Chenu C.,
Kurihara N.,
Mundy G.R.,
Roodman G. David
Publication year - 1990
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650050703
Subject(s) - multinucleate , prostaglandin e2 , osteoclast , prostaglandin , cell culture , mediator , endocrinology , prostaglandin e , transforming growth factor beta , cell growth , biology , medicine , bone marrow , transforming growth factor , microbiology and biotechnology , cell , chemistry , immunology , in vitro , biochemistry , genetics
Prostaglandins are important local regulators of bone cell function and have been shown to have multiple effects on osteoclasts. Using a human bone marrow culture system in which multinucleated cells with osteoclast characteristics form, we have recently shown that TGF‐β is a potent inhibitor of osteoclastlike cell formation and appears to act at several stages of their development. Because it has been suggested that the effects of TGF‐β are mediated via a prostaglandin‐dependent mechanism, we determined the effects of prostaglandin E 2 (PGE 2 ) on total and osteoclastlike cell formation (detected by reactivity with the 23c6 monoclonal antibody, which identifies osteoclasts) in human marrow cultures and tested whether prostaglandin synthesis was responsible for the inhibitory effects of TGF‐β on multinucleated cell formation. These studies show that PGE 2 is a potent inhibitor of both 23c6‐positive and negative multinucleated cell formation in human marrow cultures and that the effects of TGF‐β on multinucleated cell formation are not mediated by PGE 2 .