A fibronectin fragment induces type II collagen degradation by collagenase through an interleukin-1?mediated pathway

Yasuda, Tadashi; Poole, A. Robin

doi:10.1002/1529-0131(200201)46:1<138::aid-art10051>3.0.co;2-k

Cited by 115 publications

(111 citation statements)

References 54 publications

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“…Other extracellular matrix receptors, such as integrins, also play a role in the activation of MMPs. For example, extracellular fibronectin fragments activate MMPs through an IL-1-mediated pathway (41,42). Moreover, the transcription factor AP-1 is involved in the induction of MMPs by IL-1 (33).…”

Section: Discussionmentioning

confidence: 99%

Hyaluronan oligosaccharide–induced activation of transcription factors in bovine articular chondrocytes

Ohno¹,

Im²,

Knudson³

et al. 2005

Arthritis & Rheumatism

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Objective. To document the activity profile of transcription factors following chondrocyte stimulation with hyaluronan (HA) hexasaccharides (HA 6 ) and to determine the expression of genes whose transcriptional activation is tightly associated with the transcription factors.Methods. Nuclear extracts from bovine articular chondrocytes treated with HA 6 were subjected to transcription factor protein-DNA array analysis. Electrophoretic mobility shift assay (EMSA) analyses were performed to confirm the results of protein-DNA array. The gene expressions of matrix metalloproteinase 3 (MMP-3), type II collagen, and cartilage oligomeric matrix protein (COMP) were examined by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR), and protease activity was assessed by casein zymography.Results. In the protein-DNA array analysis, 12 transcription factors were up-regulated and 2 transcription factors were down-regulated in the chondrocytes treated with HA 6 . The transcription factors retinoic acid receptor (RAR), retinoid X receptor (RXR), and Sp-1 exhibited >2-fold increased activity by HA 6 treatment, as confirmed by EMSA. RT-PCR analysis showed that the expression levels of MMP-3, type II collagen, and COMP messenger RNA, which are tightly associated with the activation of RAR, RXR, or Sp-1, were upregulated by treatment with HA 6 . Addition of high molecular mass HA after HA 6 treatment resulted in abrogation of the MMP-3 induction. Conclusion.These results suggest that HA 6 increase the activity of multiple transcription factors in chondrocytes and signal the enhanced expression of key genes involved in cartilage-matrix remodeling and turnover. The data also demonstrate that high molecular mass HA has a potential to suppress the signaling activated by HA 6 .The glycosaminoglycan hyaluronan (HA) is a critical component of the extracellular matrix of articular cartilage. HA serves as a scaffold for the aggregation of cartilage proteoglycan (1) and, in this manner, forms a continuum of structure throughout the extracellular matrix. In addition, we have shown that HA facilitates the anchorage of these proteoglycan aggregates to the chondrocyte cell surface via its interaction with the membrane HA receptor CD44 (2-4). Thus, it is, in part, the interaction of chondrocytes directly with HA that constitutes the cell-matrix interaction that serves to regulate many aspects of chondrocyte metabolism (5). We have shown previously that one method of interference with the cell-matrix interactions of chondrocytes is through the use of excess small HA oligosaccharides, such as HA hexasaccharides (HA 6 ) (2,4,6). HA 6 compete with high molecular mass HA for CD44 binding; yet, they are too small in size to interfere with HA aggrecan or HA-link protein interactions (1,7,8).The consequences of this loss of cell-matrix interactions can be dramatic. In a previous study, we demonstrated that the addition of small HA oligosaccharides to human or bovine articular cartilage slices resulted in the apparent activation o...

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Section: Discussionmentioning

confidence: 99%

Hyaluronan oligosaccharide–induced activation of transcription factors in bovine articular chondrocytes

Ohno¹,

Im²,

Knudson³

et al. 2005

Arthritis & Rheumatism

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“…The initial inducers of cartilage catabolism in OA have not been identified. Potential stimuli include mechanical stress [50,51], and degradation products of ECM components including fibronectin fragments which stimulate production of matrix-degrading proteases [52][53][54][55]. IL-1 is a prototypical proinflammatory cytokine implicated in OA cartilage degradation which stimulates production of matrix metalloproteinases (MMPs).…”

Section: Cytokines Oxidative Damage and Chemokinesmentioning

confidence: 99%

Cartilage tissue engineering for degenerative joint disease☆

Nešić

Whiteside

Brittberg

et al. 2006

Advanced Drug Delivery Reviews

208

156

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Pain in the joint is often due to cartilage degeneration and represents a serious medical problem affecting people of all ages. Although many, mostly surgical techniques, are currently employed to treat cartilage lesions, none has given satisfactory results in the long term. Recent advances in biology and material science have brought tissue engineering to the forefront of new cartilage repair techniques. The combination of autologous cells, specifically designed scaffolds, bioreactors, mechanical stimulations and growth factors together with the knowledge that underlies the principles of cell biology offers promising avenues for cartilage tissue regeneration. The present review explores basic biology mechanisms for cartilage reconstruction and summarizes the advances in the tissue engineering approaches. Furthermore, the limits of the new methods and their potential application in the osteoarthritic conditions are discussed.

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“…Overall, this ongoing molecular destruction of the cartilage matrix is mainly driven by an increased activity of now partly identified proteases: the matrixmetalloproteinases (MMPs-2, -3, -13, …) and the so called aggrecanases of the ADAMTS-family of proteases (most likely ADAMTS-4 and -5). These enzymes are induced by catabolic cytokines such as IL-1 or TNFα, but also by matrix degradation products (Homandberg et al, 1998;Yasuda et al, 2002) and other non-physiologic stimuli, which the cells are exposed to. Recently, also epigenetic regulation of protease expression was reported in osteoarthritic versus normal articular cartilage (Roach et al, 2005).…”

Section: Il-1ß and Bmps -Interactive Players Of Cartilage Matrix Degrmentioning

confidence: 99%

IL-1ß and BMPs - Interactive players of cartilage matrix degradation and regeneration

Aigner

Söeder²,

Haag³

2006

eCM

100

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Intact human adult articular cartilage is central for the functioning of the articulating joints. This largely depends on the integrity of its extracellular matrix, given the high loading forces during movements in particular in the weight-bearing joints. Unlike the first impression of a more or less static tissue, articular cartilage shows -albeit in the adult organism -a slow tissue turnover. Thus, one of the most important questions in osteoarthritis research is to understand the balance of catabolic and anabolic factors in articular cartilage as this is the key to understand the biology of cartilage maintenance and degeneration.Anabolic and catabolic pathways are very much intermingled in articular cartilage. The balance between anabolism and catabolism is titrated on numerous levels, starting from the mediator-synthesizing cells which express either catabolic or anabolic factors. Also, on the level of the effector cells (i.e. chondrocytes) anabolic and catabolic gene expression compete for a balance of matrix homeostasis, namely the synthesis of matrix components and the expression and activation of matrix-degrading proteases. Also, there are multiple layers of intracellular cross-talks in between the anabolic and catabolic signalling pathways. Maybe the most important lesson from this overview is the notion that the anabolic-catabolic balance as such counts and not so much sufficient net anabolism or limited catabolism alone. Thus, it might be neither the aim of osteoarthritis therapy to foster anabolism nor to knock down catabolism, but the balance of anabolic-catabolic activities as a total needs proper titration and balancing.

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A fibronectin fragment induces type II collagen degradation by collagenase through an interleukin-1?mediated pathway

Cited by 115 publications

References 54 publications

Hyaluronan oligosaccharide–induced activation of transcription factors in bovine articular chondrocytes

Hyaluronan oligosaccharide–induced activation of transcription factors in bovine articular chondrocytes

Cartilage tissue engineering for degenerative joint disease☆

IL-1ß and BMPs - Interactive players of cartilage matrix degradation and regeneration

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