Document Detail


Fibroblast growth factor control of cartilage homeostasis.
MedLine Citation:
PMID:  23060229     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Osteoarthritis (OA) and degenerative disc disease (DDD) are similar diseases involving the breakdown of cartilage tissue, and a better understanding of the underlying biochemical processes involved in cartilage degeneration may allow for the development of novel biologic therapies aimed at slowing the disease process. Three members of the fibroblast growth factor (FGF) family, FGF-2, FGF-18, and FGF-8, have been implicated as contributing factors in cartilage homeostasis. The role of FGF-2 is controversial in both articular and intervertebral disc (IVD) cartilage as it has been associated with species- and age-dependent anabolic or catabolic events. Recent evidence suggests that FGF-2 selectively activates FGF receptor 1 (FGFR1) to exert catabolic effects in human articular chondrocytes and IVD tissue via upregulation of matrix-degrading enzyme production, inhibition of extracellular matrix (ECM) accumulation and proteoglycan synthesis, and clustering of cells characteristic of arthritic states. FGF-18, on the other hand, most likely exerts anabolic effects in human articular chondrocytes by activating the FGFR3 pathway, inducing ECM formation and chondrogenic cell differentiation, and inhibiting cell proliferation. These changes result in dispersed chondrocytes or disc cells surrounded by abundant matrix. The role of FGF-8 has recently been identified as a catabolic mediator in rat and rabbit articular cartilage, but its precise biological impact on human adult articular cartilage or IVD tissue remains unknown. The available evidence reveals the promise of FGF-2/FGFR1 antagonists, FGF-18/FGFR3 agonists, and FGF-8 antagonists (i.e., anti-FGF-8 antibody) as potential therapies to prevent cartilage degeneration and/or promote cartilage regeneration and repair in the future.
Authors:
M B Ellman; D Yan; K Ahmadinia; D Chen; H S An; H J Im
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  114     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-02-20     Completed Date:  2013-09-25     Revised Date:  2014-07-14    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  735-42     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cartilage, Articular / metabolism*,  pathology
Cell Differentiation
Chondrocytes / metabolism,  pathology
Chondrogenesis
Extracellular Matrix / metabolism
Fibroblast Growth Factor 2 / metabolism*
Fibroblast Growth Factor 8 / metabolism
Fibroblast Growth Factors / metabolism
Homeostasis*
Humans
Intervertebral Disc / metabolism,  pathology
Intervertebral Disc Degeneration / metabolism,  pathology*
Phosphorylation
Receptor, Fibroblast Growth Factor, Type 1 / metabolism
Signal Transduction
Grant Support
ID/Acronym/Agency:
R01 AR053220/AR/NIAMS NIH HHS; R01 AR054465/AR/NIAMS NIH HHS; R01 AR055915/AR/NIAMS NIH HHS; R01 AR062136/AR/NIAMS NIH HHS; R01 AR062136/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/FGF8 protein, human; 0/fibroblast growth factor 18; 103107-01-3/Fibroblast Growth Factor 2; 148997-75-5/Fibroblast Growth Factor 8; 62031-54-3/Fibroblast Growth Factors; EC 2.7.10.1/FGFR1 protein, human; EC 2.7.10.1/Receptor, Fibroblast Growth Factor, Type 1
Comments/Corrections

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