Interleukin-1-induced alterations in proteoglycan metabolism and matrix assembly

Chandrasekhar, Srinivasan; Phadke, Kalindi

doi:10.1016/0003-9861(88)90131-2

Cited by 22 publications

(15 citation statements)

References 27 publications

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“…Chondrocytes respond to IL-1 by the release of hydrolases [33] and in turn an increase of proteoglycan degradation [13,14]. Furthermore, proteoglycan synthesis is impaired [34].…”

Section: Resultsmentioning

confidence: 99%

“…This balance is disturbed in rheumatoid arthritis and other inflammatory or degenerative joint diseases [3,4]. Recent studies from several laboratories have demonstrated that the steady state metabolism of chondrocytes is affected by factors such as insulin-like growth factors IGF-I and IGF-II [5,6], transforming growth factor [7,8], and interleukin-1 (IL-1) [9][10][11][12][13][14][15]. Increased concentrations of interleukin-6 have been found in the synovial fluid of patients with osteoarthritis, rheumatoid arthritis, and crystal-related joint diseases [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

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Interleukin‐1β induces synthesis and secretion of interleukin‐6 in human chondrocytes

et al. 1990

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Increased concentrations of interleukin‐6 (IL‐6) have been found in the synovial fluid of patients with osteoarthritis, rheumatoid arthritis and crystal‐related joint deseases. It is therefore of great interest to identify the cells responsible for the production of IL‐6, and to investigate whether IL‐6 plays a role in the pathogenesisof degenerative or inflammatory joint diseases. Here we show that human interleukin‐1β (IL‐1β) induces IL‐6 synthesis and secretion in differentiated human chondrocytes. In organ cultures resembling closely the in vivo system 106 chondrocytes incubated with 100 units of interleukin‐1β per ml of medium led to the release of 6 × 103 units of IL‐6 within 24 h. Chondrocytes cultured in agarose or as monolayers similary incubated with IL‐1β produced even higher amounts of IL‐6: 70 × 103 units per 106 cells within 24 h. The induction of IL‐6 synthesis by IL‐1β was also shown at the mRNA level. IL‐6 secreted by stimulated chondrocytes showed heterogeneity upon Western blot analysis.

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“…Chondrocytes respond to IL-1 by the release of hydrolases [33] and in turn an increase of proteoglycan degradation [13,14]. Furthermore, proteoglycan synthesis is impaired [34].…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interleukin‐1β induces synthesis and secretion of interleukin‐6 in human chondrocytes

et al. 1990

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“…Hyaluronate-Sepharose Affinity Chromatography-In order to verify the aggrecan nature of the molecules, sulfate-labeled samples were evaluated by chromatography on a hyaluronate-Sepharose column (15). In brief, human umbilical cord hyaluronic acid (Sigma) was purified from sulfated glycosaminoglycans by cetyl pyridinium chloride precipitation and was coupled to EAH-Sepharose 4B (Amersham Pharmacia Biotech) using a published procedure (16).…”

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confidence: 99%

Parathyroid Hormone-(1–34) Enhances Aggrecan Synthesis via an Insulin-like Growth Factor-I Pathway

Frolik

Chandrasekhar

1999

Journal of Biological Chemistry

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During endochondral bone formation, the growth plate chondrocytes proliferate, become hypertrophic, lose the cartilage phenotype, undergo mineralization, and provide a scaffold upon which subsequent longitudinal bone growth occurs. Parathyroid hormone (PTH), a calcium-regulating hormone, and parathyroid hormone-related peptide (PTHrP), which shares several properties with PTH, have profound effects on skeletal growth and new bone formation. In order to define further the mechanism by which PTH/PTHrP promotes the cartilage phenotype, chondrocytes isolated from the rib cages of developing rat embryos were evaluated for the biosynthesis of aggrecan. Cells treated with PTH-(1-34) for a 4-h period followed by a 20-h recovery period showed a significant increase in cartilage proteoglycan (aggrecan) synthesis in a dose-dependent manner. Only N-terminally intact PTH and PTHrP were effective in stimulating aggrecan synthesis. Addition of a neutralizing antibody to insulin-like growth factor-I (IGF-I) during PTH treatment resulted in the inhibition of PTHstimulated aggrecan synthesis, whereas the addition of a neutralizing antibody to insulin-like growth factorbinding protein-2 (IGFBP-2) resulted in an increase in synthesis in both the control and PTH-treated cells. In addition, PTH treatment resulted in an increase in the mRNA for aggrecan, a reduction in IGFBP-3 mRNA, and no discernible changes in IGF-I mRNA levels, which was complemented by quantitative changes in IGFBP-3 and free IGF-I levels. The reciprocal relationship in the expression of aggrecan and IGFBP was further confirmed in chondrocytes from various gestational stages during normal development. Collectively, our results indicate that the effect of PTH may be mediated at least in part through the regulation of the IGF/IGFBP axis, by a decrease in the level of IGFBP-3, and an increase in free IGF-I levels. It is likely that the local increase in IGF-I may lead to an increase in cartilage type proteoglycan synthesis and maintenance of the cartilage phenotype.

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“…IL-1 derived from many cells, including the synovium and the chondrocytes is considered the predominant catabolic mediator responsible for cartilage degradation [9]. IL-1 has been documented to stimulate chondrocyte production of metalloproteinases [5,16,19], and to inhibit the synthesis of collagen and proteoglycans by chondrocytes [19,24]. This study has clearly demonstrated the release of proteoglycans from the pellet mass into the tissue culture media by enzymatic degradation of ECM as induced by IL-1α, in which they were detected as GAG.…”

Section: Discussionmentioning

confidence: 99%

Consideration of the Role of Antigenic Keratan Sulphate Reacting to a 1/14/16H9 Antibody as a Molecular Marker to Monitor Cartilage Metabolism in Horses

Okumura

Tagami²,

Fujinaga

2000

The Journal of Veterinary Medical Science

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ABSTRACT. The role of keratan sulphate (KS) as a marker of cartilage metabolism was evaluated by using an in vitro model of equine articular cartilage. Articular cartilage was harvested from clinically healthy 6-month-old foals (n=3). Chondrocytes were centrifuged and cultured as pellets. Chondrocyte pellets were stimulated by insulin-like growth factor (IGF)-Iα or interleukin (IL)-1α for 2 weeks. The sulfated glycosaminoglycans (GAG) and antigenic KS concentrations in the culture media were measured by a 1,9-dimethyl-methylene blue (DMMB) colorimetric assay and an inhibition ELISA using a 1/14/16H9 antibody, respectively. Concentration of GAG was significantly increased in the media of pellets stimulated by both IGF-Iα and IL-1α. Antigenic KS concentration was significantly increased in those stimulated by IL-1α, while no significant change was found in those stimulated by IGF-Iα. A high correlation between GAG and antigenic KS concentrations was found in the media of pellets stimulated by IL-1α (r=0.87), but not in those stimulated by IGF-Iα (r=0.43). The results suggest that the concentration of antigenic KS reacting to 1/14/16H9 mirrors the GAG concentration during the stage of cartilage catabolism, but not during the cartilage anabolic stage. The concentration of antigenic KS reacting to 1/14/16H9 antibody in biological fluids could therefore be a useful marker to further understand principally the catabolic and slightly the anabolic process of articular cartilage metabolism.-KEY WORDS: cartilage metabolism, chondrocyte, equine, joint, keratan sulphate.

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Interleukin-1-induced alterations in proteoglycan metabolism and matrix assembly

Cited by 22 publications

References 27 publications

Interleukin‐1β induces synthesis and secretion of interleukin‐6 in human chondrocytes

Interleukin‐1β induces synthesis and secretion of interleukin‐6 in human chondrocytes

Parathyroid Hormone-(1–34) Enhances Aggrecan Synthesis via an Insulin-like Growth Factor-I Pathway

Consideration of the Role of Antigenic Keratan Sulphate Reacting to a 1/14/16H9 Antibody as a Molecular Marker to Monitor Cartilage Metabolism in Horses

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