Publication: Anabolic actions of IGF-I and TGF-B1 on Interleukin-1B-treated human articular chondrocytes: Evaluation in two and three dimensional cultures
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Date
2009
Authors
Seifarth, Claudia ; Csaki, Constanze ; Shakibaei, Mehdi
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Pro-inflammatory cytokines, such as
interleukin-1ß (IL-1ß) and tumor necrosis factor-a
(TNF-a) play a key role in the pathogenesis of
Osteoarthritis (OA). The aim of this study was to
investigate the potential anti-inflammatory properties of
the growth factors IGF-I and/or TGF-ß1 on IL-1ß
signalling pathways and their effect on the chondrogenic
potential of dedifferentiated human articular
chondrocytes in vitro.
Serum-starved human articular chondrocytes were
treated with IL-1ß to induce dedifferentiation and further
treated with IGF-I and/or TGF-ß1 at various
concentrations. The effects of growth factors were
evaluated both in monolayer and high-density cultures.
Incubation with the cytokine IL-1ß resulted in rapid
dedifferentiation of the cells; they lost their chondrocytelike
phenotype while down-regulating the expression of
collagen type II, integrin, extracellular regulated kinase
(Erk 1/2) and the chondrogenic transcription factor
Sox9. Co-treatment with IGF-I and/or TGF-ß1
stimulated the cells to redifferentiate, increasing the
expression of the above-mentioned cartilage-specific
proteins. These events correlated with down-regulation
of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-
13 (MMP-13). Furthermore, in high-density
cultures, we observed evidence for new cartilage
formation after co-treatment with these growth factors.
We further detected that all examined proteins were
more strongly expressed during combination treatment.
These results indicate that IGF-I and TGF-ß1 exert
additive anabolic effects on chondrocytes and may
stabilize the chondrogenic potential. The additive action
of these growth factors on chondrocytes may find practical applications in the fields of OA and cartilage
tissue engineering.
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