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(Received for publication, April 9, 1996, and in revised form, July 9, 1996)
From the Division of Bone and Mineral Diseases and the
To analyze how estrogen blocks
osteoclastogenesis, we investigated the effects of ovariectomy on
osteoclast (OC) formation in co-cultures of purified OC precursors and
purified stromal cells (SC). OC formation was higher in co-cultures
containing SC from ovariectomized mice than in those containing SC from
sham-operated mice, thus suggesting that estrogen regulates
osteoclastogenesis by targeting SC. Ovariectomy also increased the
mononuclear cell secretion of interleukin (IL)-1) and tumor necrosis
factor (TNF) and the SC production of macrophage colony-stimulating
factor (MCSF). Osteoclastogenesis and SC production of M-CSF were
not blocked by in vitro estrogen treatment but were
decreased by in vivo treatment of donor mice with either
estrogen or a combination of the IL-1 inhibitor, IL-1 receptor
antagonist, and the TNF inhibitor, TNF binding protein. IL-1 and TNF
production were also blocked by in vivo estrogen treatment,
demonstrating that the increased bone marrow levels of IL-1 and TNF
characteristic of ovariectomized mice induce the formation of a SC
population characterized by a high production of M-CSF and increased
pro-osteoclastogenic activity. Since in co-cultures of SC and OC
precursors M-CSF levels correlated with OC production
(r = 0.7, p < 0.0001), the data also
indicate that the pro-osteoclastogenic activity of SC is proportional
to their secretion of M-CSF. The ability of estrogen to decrease SC
production of M-CSF and the pro-osteoclastogenic activity of these
cells by regulating IL-1 and TNF production is a previously undescribed
mechanism by which estrogen down-regulates osteoclastogenesis.
Volume 271, Number 46,
Issue of November 15, 1996
pp. 28890-28897
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
,
Department of Pathology, Washington University School of
Medicine and Barnes/Jewish Hospital, St. Louis, Missouri 63110
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