Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 394, Issue 1, Pages 6-11Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.02.113
Keywords
Osteoporosis; Osteoclast; FSH; Gonadotropin; Bone loss
Categories
Funding
- National Institute on Aging [AG23176]
- National Institutes of Health [DK70526, DK80490, AR053976, AR055208, AR053566]
- Department of Veterans Affairs
- American Federation for Aging Research
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We confirm that FSH stimulates osteoclast formation, function and survival to enhance bone resorption. It does so via the activation of a pertussis toxin-sensitive G(i)-coupled FSH receptor that we and others have identified on murine and human osteoclast precursors and mature osteoclasts. FSH additionally enhances the production of several osteoclastogenic cytokines, importantly TNF alpha, likely within the bone marrow microenvironment, to augment its pro-resorptive action. FSH levels in humans rise before estrogen falls, and this hormonal change coincides with the most rapid rates of bone loss. On the basis of accumulating evidence, we reaffirm that FSH contributes to the rapid pen-menopausal and early post-menopausal bone loss, which might thus be amenable to FSH blockade. (C) 2010 Elsevier Inc. All rights reserved.
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