Hypoxia-Induced Fibroblast Growth Factor 11 Stimulates Osteoclast-Mediated Resorption of Bone

Over-activation of osteoclasts is directly responsible for pathological bone loss in conditions such as rheumatoid arthritis and cancer metastasis to bone. Hypoxia is a common feature of these conditions, associated with poor prognosis, which also stimulates osteoclast-mediated bone resorption via i...

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Bibliographic Details
Published in:Calcified tissue international 2017-04, Vol.100 (4), p.382-391
Main Author: Knowles, Helen J.
Format: Article
Language:English
Subjects:
Biochemistry
Biomedical and Life Sciences
Bone and Bones - metabolism
Bone Resorption - metabolism
Bones
Cell Biology
Cell Differentiation - drug effects
Cell Hypoxia
Cells, Cultured
Endocrinology
Fibroblast Growth Factors - genetics
Fibroblast Growth Factors - metabolism
Fibroblasts
Growth factors
Humans
Life Sciences
Original Research
Orthopedics
Osteoclasts - metabolism
Rheumatoid arthritis
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Summary:Over-activation of osteoclasts is directly responsible for pathological bone loss in conditions such as rheumatoid arthritis and cancer metastasis to bone. Hypoxia is a common feature of these conditions, associated with poor prognosis, which also stimulates osteoclast-mediated bone resorption via induction of the hypoxia-inducible transcription factor HIF-1α. Here, we investigate the effects of fibroblast growth factor 11 (FGF11) on osteoclast function. FGF11 is an intracellular FGF that was induced both by hypoxia (2% O 2 , p  
ISSN:0171-967X
1432-0827
DOI:10.1007/s00223-016-0228-1