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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2006-4-24
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pubmed:abstractText |
Postmenopausal osteoporosis, a global public health problem, has for decades been attributed solely to declining estrogen levels. Although FSH levels rise sharply in parallel, a direct effect of FSH on the skeleton has never been explored. We show that FSH is required for hypogonadal bone loss. Neither FSHbeta nor FSH receptor (FSHR) null mice have bone loss despite severe hypogonadism. Bone mass is increased and osteoclastic resorption is decreased in haploinsufficient FSHbeta+/- mice with normal ovarian function, suggesting that the skeletal action of FSH is estrogen independent. Osteoclasts and their precursors possess G(i2alpha)-coupled FSHRs that activate MEK/Erk, NF-kappaB, and Akt to result in enhanced osteoclast formation and function. We suggest that high circulating FSH causes hypogonadal bone loss.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0092-8674
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pubmed:author |
pubmed-author:BlairHarry CHC,
pubmed-author:BraunJonathanJ,
pubmed-author:Cardoso-LandaLuisL,
pubmed-author:IqbalJameelJ,
pubmed-author:KUY CYC,
pubmed-author:KumarT RajendraTR,
pubmed-author:MoongaBaljit SBS,
pubmed-author:PapachristouDionysios JDJ,
pubmed-author:PengYuanzhenY,
pubmed-author:SairamM RamMR,
pubmed-author:SchafflerMitchell BMB,
pubmed-author:SharrowAllison CAC,
pubmed-author:VioMM,
pubmed-author:YaroslavskiyBeatrice BBB,
pubmed-author:ZaidiMoneM,
pubmed-author:ZaidiSamirS,
pubmed-author:ZalloneAlbertaA,
pubmed-author:ZhiyuanZhangZ,
pubmed-author:ZhouHangH,
pubmed-author:ZhuLing-LingLL
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pubmed:issnType |
Print
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pubmed:day |
21
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pubmed:volume |
125
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
247-60
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16630814-Animals,
pubmed-meshheading:16630814-Bone Resorption,
pubmed-meshheading:16630814-Bone and Bones,
pubmed-meshheading:16630814-Cell Differentiation,
pubmed-meshheading:16630814-Cells, Cultured,
pubmed-meshheading:16630814-Enzyme Activation,
pubmed-meshheading:16630814-Estrogens,
pubmed-meshheading:16630814-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:16630814-Female,
pubmed-meshheading:16630814-Follicle Stimulating Hormone,
pubmed-meshheading:16630814-GTP-Binding Protein alpha Subunit, Gi2,
pubmed-meshheading:16630814-Humans,
pubmed-meshheading:16630814-Hypogonadism,
pubmed-meshheading:16630814-Mice,
pubmed-meshheading:16630814-Mice, Inbred C57BL,
pubmed-meshheading:16630814-Mice, Knockout,
pubmed-meshheading:16630814-NF-kappa B,
pubmed-meshheading:16630814-Osteoclasts,
pubmed-meshheading:16630814-Osteoporosis,
pubmed-meshheading:16630814-Protein Subunits,
pubmed-meshheading:16630814-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:16630814-Receptors, FSH,
pubmed-meshheading:16630814-Signal Transduction
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pubmed:year |
2006
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pubmed:articleTitle |
FSH directly regulates bone mass.
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pubmed:affiliation |
Mount Sinai Bone Program, Department of Medicine and Department of Orthopedics, Mount Sinai School of Medicine, New York, NY 10029, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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