The effect of interleukin‐1 on cytokine gene expression in cultured human articular chondrocytes analyzed by messenger rna phenotyping

Seid, J. M.; Rahman, Shamim; Graveley, R.; Bunning, R.A.D.; Nordmann, R.; Wishart, William L.; Russell, R.G.G.

doi:10.1002/art.1780360107

Cited by 19 publications

(4 citation statements)

References 32 publications

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“…Under our experimental conditions, control osteoblast TGFβ 1 mRNA was not sufficient to be quantified, which is in agreement with the results of other authors for normal tissues (Weyand et al 1994). Growth factor mRNAs are not always detectable but are inducible by the stimulus of other growth factors or by varying the culture conditions (Seid et al 1993). In Apert osteoblasts an elevated amount of TGFβ 1 mRNA expression was observed, and this was greater in ASO than in APO.…”

Section: Discussionsupporting

confidence: 92%

Differential in vitro phenotype pattern, transforming growth factor-β 1 activity and mRNA expression of transforming growth factor-β 1 in Apert osteoblasts

Locci

Baroni

Pezzetti

et al. 1999

Cell and Tissue Research

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The phenotype of Apert osteoblasts differs from that of normal osteoblasts in the accumulation of macromolecules in the extracellular matrix. Apert osteoblasts increase type I collagen, fibronectin and glycosaminoglycans secretion compared with normal osteoblasts. Because the extracellular matrix macromolecule accumulation is greatly modulated by transforming growth factor-beta(1), we examined the ability of normal and Apert osteoblasts to secrete transforming growth factor-beta(1) by CCL-64 assay and to produce transforming growth factor-beta(1 )by analysis of the mRNA expression of transforming growth factor-beta(1). Northern blot analysis revealed an increased amount of transforming growth factor-beta(1) mRNA expression in Apert osteoblasts compared with normal ones. Moreover, the level of the active transforming growth factor-beta(1) isoform was higher in Apert than in normal media. In pathologic cells, the increase in transforming growth factor-beta(1) gene expression was associated with a parallel increase in the factor secreted into the medium. The level of transforming growth factor-beta(1) was decreased by the addition of basic fibroblast growth factor. Transforming growth factor-beta(1) is controlled temporally and spatially during skeletal tissue development and produces complex stimulatory and inhibitory changes in osteoblast functions. We hypothesise that in vitro differences between normal and Apert osteoblasts may be correlated to different transforming growth factor-beta(1) cascade patterns, probably due to an altered balance between transforming growth factor-beta(1) and basic fibroblast growth factor.

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Section: Discussionsupporting

confidence: 92%

Differential in vitro phenotype pattern, transforming growth factor-β 1 activity and mRNA expression of transforming growth factor-β 1 in Apert osteoblasts

Locci

Baroni

Pezzetti

et al. 1999

Cell and Tissue Research

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“…In accordance with the findings of Pohlers et al (6), we demonstrated increased levels of all markers except TNFα and increased gene expression of VEGF and IL‐6 in synovial membrane. Other investigators have demonstrated up‐regulation of cytokine production in chondrocytes of patients with arthritis (47). In the present study, IGF‐1 protein concentrations were increased in both synovial membrane and cartilage from knees with AIA.…”

Section: Discussionmentioning

confidence: 97%

Intraarticular injection of platelet‐rich plasma reduces inflammation in a pig model of rheumatoid arthritis of the knee joint

Lippross¹,

Moeller²,

Haas³

et al. 2011

Arthritis & Rheumatism

102

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Objective. Treatment options for rheumatoid arthritis range from symptomatic approaches to modern molecular interventions such as inhibition of inflammatory mediators. Inhibition of inflammation by plateletrich plasma (PRP) has been proposed as a treatment for tendinitis and osteoarthritis. The present study was undertaken to investigate the effect of PRP on antigeninduced arthritis (AIA) of the knee joint in a large animal model.Methods. Six-month-old pigs (n ‫؍‬ 10) were systemically immunized by bovine serum albumin (BSA) injection, and arthritis was induced by intraarticular BSA injection. PRP was injected into the knee joints of 5 of the animals after 2 weeks. An additional 5 animals received no systemic immunization (controls). Signs of arthritis were documented by plain histologic analysis, Safranin O staining, and immunohistochemistry analysis for type II collagen (CII), interleukin-6 (IL-6), and vascular endothelial growth factor (VEGF). Interleukin-1␤ (IL-1␤), IL-6, tumor necrosis factor ␣ (TNF␣), VEGF, and insulin-like growth factor 1 (IGF-1) protein content was measured by Luminex assay.Results. In the pigs with AIA, plain histologic analysis revealed severe arthritic changes in the synovium. Safranin O and CII staining showed decreased proteoglycan and CII content in cartilage. Immunohistochemistry analysis revealed increased levels of IL-6 and VEGF in synovium and cartilage, and protein concentrations of IL-6, VEGF, IL-1␤, and IGF-1 in synovium and cartilage were elevated as well; in addition, TNF␣ protein was increased in cartilage. Treatment with PRP led to attenuation of these arthritic changes in the synovium and cartilage. Conclusion. We have described a porcine model of AIA. Experiments using this model demonstrated that PRP can attenuate arthritic changes as assessed histologically and based on protein synthesis of typical inflammatory mediators in the synovial membrane and cartilage.

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“…The inducibility of CSFs in chondrocytes has been well studied [8][9][10][11], and the variability found among the human samples may reflect different stages of chondrocyte activation or development. In contrast, TNF-fl, generally known as a lymphotoxin, has not been reported to be found in chondrocytes, but like TNF-a, it is extremely pleiotropic [25].…”

Section: Discussionmentioning

confidence: 99%

“…Chondrocytes produce an array of cytokines including IL-1 [4], IL-6 [5], IL-8 [6], IL-11 [7], granulocyte colony stimulating factor (G-CSF) [8,9], granulocyte macrophage colony stimulating factor (GM-CSF) [8][9][10], and macrophage colony stimulating factor (M-CSF) [11], some of which are constitutive and may have maintenance functions. Others are inducible and also may be under autocrine control.…”

Section: Introductionmentioning

confidence: 99%

Cytokine mRNA repertoire of articular chondrocytes from arthritic patients, infants, and neonatal mice

et al. 1996

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Articular chondrocytes from nine arthritic patients, five infants, and Balb/c neonatal mice were analyzed for the presence of various cytokine mRNAs by a reverse transcriptase polymerase chain reaction (RT-PCR). Four cytokine mRNAs, interleukin (IL)-6, IL-8, IL-11, and macrophage colony stimulating factor (M-CSF), were detected in all human chondrocytes, regardless of source. IL-10, IL-12p35, and tumor necrosis factor alpha (TNF-alpha) transcripts were found in at least 12 of the 14 human samples. IL-13, granulocyte colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor (GM-CSF), and TNF-beta mRNAs were found more predominantly in infant samples and in samples from patients with rheumatoid arthritis (RA) compared with samples from patients with osteoarthritis (OA). Another group of cytokine mRNAs, IL-1 (alpha, beta), IL-4, IL-5, and IL-7, were only weakly expressed in some human samples. The cytokine transcripts that were not found were IL-2, IL3, and interferon gamma (IFN-gamma). Because of the large array of cytokine transcripts detected, human chondrocyte preparations were further purified by reacting them with a monoclonal antibody specific to chondrocyte differentiation antigen and subjecting them to fluorescent-activated cell sorting. A similar array of cytokines was found between the sorted and unsorted chondrocytes, although TNF-alpha, G-CSF and GM-CSF transcripts appeared to be upregulated during the sorting process. Human chondrocytes that dedifferentiated into fibroblasts (a 40-day and a 77-day culture) no longer expressed mRNAs for IL-1, G-CSF, GM-CSF, and TNF-alpha, but all other cytokine mRNAs remained detectable. Although certain phenotypic characteristics were lost, including reactivity to chondrocyte-specific monoclonal antibodies and morphological features, chondrocytes in long-term culture still expressed cytokine mRNAs. As expected, more consistent results were obtained when seven preparations of chondrocytes from neonatal Balb/c mice were examined using available cytokine primers. They contained IL-1, IL-5, IL-6, IL-7, IL-12, GM-CSF, M-CSF, transforming growth factor beta (TGF-beta), TNF-alpha, and TNF-beta mRNAs but lacked IL-2, IL-3, IL-4, IL-10, and IFN-gamma mRNAs. Future experiments to define conditions by which these cytokine protein products are expressed are needed to help assess their roles in chondrocyte biology and in disease states.

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The effect of interleukin‐1 on cytokine gene expression in cultured human articular chondrocytes analyzed by messenger rna phenotyping

Cited by 19 publications

References 32 publications

Differential in vitro phenotype pattern, transforming growth factor-β 1 activity and mRNA expression of transforming growth factor-β 1 in Apert osteoblasts

Differential in vitro phenotype pattern, transforming growth factor-β 1 activity and mRNA expression of transforming growth factor-β 1 in Apert osteoblasts

Intraarticular injection of platelet‐rich plasma reduces inflammation in a pig model of rheumatoid arthritis of the knee joint

Cytokine mRNA repertoire of articular chondrocytes from arthritic patients, infants, and neonatal mice

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