Articular chondrocytes secrete IL-1, express membrane IL-1, and have IL-1 inhibitory activity

Tiku, Katherine; Thakker‐Varia, Smita; Ramachandrula, Anand; Tiku, M. L.

doi:10.1016/0008-8749(92)90172-l

Cited by 40 publications

(28 citation statements)

References 37 publications

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“…However, TLRs not only are expressed by cells involved in activation of the immune system, but also have been found, among other molecules, in human aortic endothelial cells, lung epithelial cells, hepatocytes, and synoviocytes (36)(37)(38)(39). The observations reported herein, that TLRs are also expressed in articular chondrocytes, expand these findings and are consistent with the notion that these cells display functional properties in common with monocytes/macrophages (40)(41)(42)(43)(44)(45).…”

Section: Discussionsupporting

confidence: 88%

Toll‐like receptors and chondrocytes: The lipopolysaccharide‐induced decrease in cartilage matrix synthesis is dependent on the presence of toll‐like receptor 4 and antagonized by bone morphogenetic protein 7

Bobacz

Sunk

Hofstaetter

et al. 2007

Arthritis & Rheumatism

105

106

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Conclusion.These data demonstrate the presence of TLRs in human articular cartilage. The suppressive effects of LPS on cartilage biosynthetic activity are dependent on the presence of TLR-4, are governed, at least in part, by an up-regulation of IL-1␤, and are mediated by p38 kinase. These in vitro data indicate an anti-anabolic effect of TLR-4 in articular chondrocytes that may hamper cartilage repair in various joint diseases.

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Section: Discussionsupporting

confidence: 88%

Toll‐like receptors and chondrocytes: The lipopolysaccharide‐induced decrease in cartilage matrix synthesis is dependent on the presence of toll‐like receptor 4 and antagonized by bone morphogenetic protein 7

Bobacz

Sunk

Hofstaetter

et al. 2007

Arthritis & Rheumatism

105

106

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“…It is noteworthy in this regard that when chondrocytes were exposed rHuILlp, nascent nuclear transcripts hybridizing with pro-MMP probes were also produced (not shown), as was seen with OA chondrocyte-derived CM. It seems likely therefore that the mechanism(s) involved in these up-regulations may include a cytokine such as IL-1 that is known to be produced by chondrocytes (37).…”

Section: Discussionmentioning

confidence: 99%

Prostromelysin and procollagenase genes are differentially UP‐regulated in chondrocytes from the knees of rabbits with experimental osteoarthritis

Mehraban

Kuo

Riera

et al. 1994

Arthritis & Rheumatism

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Objective. To determine the relative expressions of matrix metalloprotease (MMP) genes pro-MMP1 and pro-MMP3 in the cartilage of rabbits with experimentally induced osteoarthritis (OA), and to assess the role of the chondrocyte in this process.Methods. OA was induced in rabbits after partial medial meniscectomy. Rabbits were killed at 4 weeks or 8 weeks, and total cellular RNA was prepared from cartilage and probed by Northern blotting with pro-MMP 32P-labeled complementary DNA. Monolayer chondrocytes were used to assess MMP-inducing activity of chondrocyte factor@).Results. Pro-MMP messenger RNAs (mRNAs) were up-regulated in experimental OA cartilage; pro-MMP3 mRNA expression exceeded that of pro-MMP1. Conditioned medium from OA-derived chondrocytes upregulated pro-MMP mRNAs in normal chondrocytes.Conclusion. Up-regulation of MMP genes in this OA model may contribute to cartilage degradation. Chondrocytes up-regulate MMP genes via an autocrine pathway .Osteoarthritis (OA), characterized by progressive destruction of articular cartilage, is purported to

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“…The chondrocytes were isolated as described previously (27). The viability of chondrocytes was confirmed by trypan blue exclusion.…”

Section: Methodsmentioning

confidence: 99%

Evidence Linking Chondrocyte Lipid Peroxidation to Cartilage Matrix Protein Degradation

Tiku¹,

Shah²,

Allison³

2000

Journal of Biological Chemistry

Self Cite

233

174

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Reactive oxygen species (ROS) are implicated in both cartilage aging and the pathogenesis of osteoarthritis. We developed an in vitro model to study the role of chondrocyte-derived ROS in cartilage matrix protein degradation. Matrix proteins in cultured primary articular chondrocytes were labeled with [ 3 H]proline, and the washed cell matrix was returned to a serum-free balanced salt solution. Exposure to hydrogen peroxide resulted in oxidative damage to the cell matrix as established by monitoring the release of labeled material into the medium. Calcium ionophore treatment of chondrocytes, in a dose-dependent manner, significantly enhanced the release of labeled matrix, suggesting a chondrocyte-dependent mechanism of matrix degradation. Antioxidant enzymes such as catalase or superoxide dismutase did not influence matrix release by the calcium ionophore-activated chondrocytes. However, vitamin E, at physiological concentrations, significantly diminished the release of labeled matrix by activated chondrocytes. The fact that vitamin E is a chain-breaking antioxidant indicates that the mechanism of matrix degradation and release is mediated by the lipid peroxidation process. Lipid peroxidation was measured in chondrocytes loaded with cis-parinaric acid. Both resting and activated cells showed constitutive and enhanced levels of lipid peroxidation activity, which were significantly reduced in the presence of vitamin E. In an immunoblot analysis, malondialdehyde and hydroxynonenal adducts were observed in chondrocyte-matrix extracts, and the amount of adducts increased with calcium ionophore treatment. Furthermore, vitamin E diminished aldehyde-protein adduct formation in activated extracts, which suggests that vitamin E has an antioxidant role in preventing protein oxidation. This study provides in vitro evidence linking chondrocyte lipid peroxidation to cartilage matrix protein (collagen) oxidation and degradation and suggests that vitamin E has a preventive role. These observations indicate that chondrocyte lipid peroxidation may have a role in the pathogenesis of cartilage aging and osteoarthritis.Cartilage degeneration is a hallmark of cartilage aging and osteoarthritis (1). Degeneration of articular cartilage in osteoarthritis is accompanied by chronic pain and significant disability. In a series of reports (2-7), we and others have documented that chondrocytes produce reactive oxygen species (ROS).1 The production of ROS by chondrocytes can contribute to degradation of the cartilage matrix. For example, ROS can mediate intracellular signaling and gene activation of cytokine and growth factor-induced products in chondrocytes (8, 9). In activated neutrophils and monocytes/macrophages, the cellspecific gene products of "NADPH-oxidase complex" physically come together and initiate single electron reduction of oxygen and the release of ROS outside the cells. Phagocytes use the toxic properties of ROS to eliminate pathogens (10, 11); in contrast, the biological role of secreted ROS in cartilage is not known.The ob...

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Articular chondrocytes secrete IL-1, express membrane IL-1, and have IL-1 inhibitory activity

Cited by 40 publications

References 37 publications

Toll‐like receptors and chondrocytes: The lipopolysaccharide‐induced decrease in cartilage matrix synthesis is dependent on the presence of toll‐like receptor 4 and antagonized by bone morphogenetic protein 7

Toll‐like receptors and chondrocytes: The lipopolysaccharide‐induced decrease in cartilage matrix synthesis is dependent on the presence of toll‐like receptor 4 and antagonized by bone morphogenetic protein 7

Prostromelysin and procollagenase genes are differentially UP‐regulated in chondrocytes from the knees of rabbits with experimental osteoarthritis

Evidence Linking Chondrocyte Lipid Peroxidation to Cartilage Matrix Protein Degradation

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