Please use this identifier to cite or link to this item: https://doi.org/10.1186/ar2474
Title: Role of fibroblast growth factor 8 (FGF8) in animal models of osteoarthritis
Authors: Uchii, M
Tamura, T
Suda, T 
Kakuni, M
Tanaka, A
Miki, I
Keywords: fibroblast growth factor 8
glycosaminoglycan polysulfate
interleukin 1alpha
iodoacetic acid
matrix metalloproteinase
monoclonal antibody
prostaglandin E2
proteinase
recombinant fibroblast growth factor
recombinant fibroblast growth factor 8
stromelysin
A73025
fibroblast growth factor 8
glycosaminoglycan
iodoacetic acid
prostaglandin E2
stromelysin
unclassified drug
animal cell
animal experiment
animal model
animal tissue
article
cartilage cell
cartilage degeneration
cell culture
cell hyperplasia
controlled study
disease exacerbation
enzyme release
enzyme synthesis
extracellular matrix
fibroblast
immunohistochemistry
knee osteoarthritis
male
meniscectomy
nonhuman
prostaglandin release
protein analysis
protein degradation
protein expression
protein function
protein secretion
rabbit
rat
synoviocyte
synovium
animal
articular cartilage
cell proliferation
chemically induced disorder
disease model
drug effect
intraarticular drug administration
knee osteoarthritis
metabolism
pathology
Sprague Dawley rat
synovium
Animals
Cartilage, Articular
Cell Proliferation
Cells, Cultured
Chondrocytes
Dinoprostone
Disease Models, Animal
Extracellular Matrix
Fibroblast Growth Factor 8
Glycosaminoglycans
Injections, Intra-Articular
Iodoacetic Acid
Male
Matrix Metalloproteinase 3
Osteoarthritis, Knee
Rabbits
Rats
Rats, Sprague-Dawley
Synovial Membrane
Issue Date: 2008
Citation: Uchii, M, Tamura, T, Suda, T, Kakuni, M, Tanaka, A, Miki, I (2008). Role of fibroblast growth factor 8 (FGF8) in animal models of osteoarthritis. Arthritis Research and Therapy 10 (4) : R90. ScholarBank@NUS Repository. https://doi.org/10.1186/ar2474
Rights: Attribution 4.0 International
Abstract: Introduction: Fibroblast growth factor 8 (FGF8) is isolated as an androgen-induced growth factor, and has recently been shown to contribute to limb morphogenesis. The aim of the present study was to clarify the role of FGF8 in animal models of osteoarthritis (OA). Methods: The expression of FGF8 in the partial meniscectomy model of OA in the rabbit knee was examined by immunohistochemistry. The effect of intraperitoneal administration of anti-FGF8 antibody was tested in a model of OA that employed injection of monoiodoacetic acid or FGF8 into the knee joint of rats. The effect of FGF8 was also tested using cultured chondrocytes. Rabbit articular chondrocytes were treated with FGF8 for 48 hours, and the production of matrix metalloproteinase and the degradation of sulfated glycosaminoglycan in the extracellular matrix (ECM) were measured. Results: The expression of FGF8 in hyperplastic synovial cells and fibroblasts was induced in the meniscectomized OA model, whereas little or no expression was detected in normal synovium. Injection of FGF8 into rat knee joints induced the degradation of the ECM, which was suppressed by anti-FGF8 antibody. In the monoiodoacetic acid-induced arthritis model, anti-FGF8 antibody reduced ECM release into the synovial cavity. In cultured chondrocytes, FGF8 induced the release of matrix metalloproteinase 3 and prostaglandin E2, and caused degradation of the ECM. The combination of FGF8 and IL-1? accelerated the degradation of the ECM. Anti-FGF8 antibody suppressed the effects of FGF8 on the cells. Conclusion: FGF8 is produced by injured synovium and enhances the production of protease and prostaglandin E2 from inflamed synoviocytes. Degradation of the ECM is enhanced by FGF8. FGF8 may therefore participate in the degradation of cartilage and exacerbation of osteoarthritis. © 2008 Uchii et al.; licensee BioMed Central Ltd.
Source Title: Arthritis Research and Therapy
URI: https://scholarbank.nus.edu.sg/handle/10635/177965
ISSN: 14786354
DOI: 10.1186/ar2474
Rights: Attribution 4.0 International
Appears in Collections:Elements
Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1186_ar2474.pdf1.22 MBAdobe PDF

OPEN

NoneView/Download

SCOPUSTM   
Citations

17
checked on Apr 15, 2021

Page view(s)

43
checked on Apr 16, 2021

Google ScholarTM

Check

Altmetric


This item is licensed under a Creative Commons License Creative Commons