Cytokines and cellular interactions in inflammatory synovitis

Arend, William P.

doi:10.1172/jci12952

Cited by 16 publications

(15 citation statements)

References 21 publications

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“…Inflammation may inhibit the synthesis of aggrecan through excessive production of pro-inflammatory cytokines [34]. Chondrocytes express several chemokines and have receptors that enable responses associated with cartilage catabolism [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Concentration of the CS-846 Epitope in Serum and Synovial Fluid of Horses with Different Grades of Osteochondral Fragments in the Carpal Joints

Chávez¹,

Folch²,

Araya³

et al. 2016

Gen Med (Los Angeles)

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The aim of this study was to determine serum and synovial concentrations of the CS-846 epitope of articular cartilage aggrecan, in horses with a radiological diagnosis of osteochondral fragmentation (OF). For this purpose, 20 thoroughbred horses with unilateral radiocarpal or intercarpal OF were used, and 10 clinically and radiologically healthy Thoroughbred horses were assigned to the control group. Serum and synovial concentrations of the CS-846 epitope were measured in both groups by means of ELISA. The concentration of the CS-846 epitope in synovial fluid was significantly higher in carpal joints with moderate articular damage (grade 2 OF) than in the control group or in horses with severe disease (grade 3 and 4 OF). In serum, non-statistical differences in the concentration of the CS-846 epitope were observed between horses with OF and controls. We conclude that the concentration of CS-846 epitope in synovial fluid suggests an increase in cartilage aggrecan synthesis, which may be associated with the presence of moderate clinical disease. The CS-846 epitope concentration in synovial fluid may be a useful biomarker for the study of carpal OF in horses, providing a measure of the balance between cartilage synthesis and degradation in this equine disease.

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Section: Discussionmentioning

confidence: 99%

Concentration of the CS-846 Epitope in Serum and Synovial Fluid of Horses with Different Grades of Osteochondral Fragments in the Carpal Joints

Chávez¹,

Folch²,

Araya³

et al. 2016

Gen Med (Los Angeles)

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“…Cytokines and chemokines are produced in inflamed joints by the synovium, macrophages and fibroblast-like synoviocytes, and they are thought to be key regulators of the inflammatory process (12, 13, 15, 22, 23). Cytokines both enhance the migration of cells into the joint and stimulate matrix metalloproteinase production in synovial fibroblasts and chondrocytes (22), and chemokines function in the recruitment of neutrophils, monocytes, immature dendritic cells, B cells and activated T cells (24). Furthermore, it has recently been reported that the CXC family of chemokines is important in the regulation of angiogenesis in rheumatoid arthritis, and CCL2, CCL3, and CCR2 stimulate osteoclastogenesis (25-27).…”

Section: Discussionmentioning

confidence: 99%

Resistin induces expression of proinflammatory cytokines and chemokines in human articular chondrocytes via transcription and messenger RNA stabilization

Zhang

Xing

Hensley

et al. 2010

Arthritis & Rheumatism

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Objective To elucidate the effect of resistin on human articular chondrocytes, and generate a picture of their regulation at the transcriptional and post-transcriptional levels. Methods Human articular chondrocytes were cultured with resistin. Changes in gene expression were analyzed at various doses and times. Cells were also treated with the transcriptional inhibitor actinomycin D after resistin treatment, or the nuclear factor kappa B (NF-κB) inhibitor IKK-NBD before resistin treatment. Gene expression was tested by quantitative real-time polymerase chain reaction. Computational analysis for transcription factor binding motifs was performed on the promoter regions of differentially expressed genes. TC28 chondrocytes were transfected with CCL3 and CCL4 promoter constructs, pNF-κB reporter, and NF-κB and CCAAT/enhancer-binding protein β (C/EBPβ) expression vectors with or without resistin. Results Resistin-treated human articular chondrocytes increased the expression of cytokines and chemokines. The mRNAs for MMP-1, MMP-13 and ADAMTS-4 also increased while COL2A1 and aggrecan were down-regulated. Cytokine and chemokine genes could be categorized into three groups according to the pattern of mRNA expression in a 24 h time course. One pattern suggested rapid regulation by mRNA stability. The second and third patterns were consistent with transcriptional regulation. Computational analysis suggested the transcription factors NF-κB and C/EBPβ were involved in the resistin-induced up-regulation. This prediction was confirmed by the co-transfection of NF-κB and C/EBPβ, and IKK-NBD inhibition. Conclusion Resistin has diverse effects on gene expression in human chondrocytes affecting chemokines, cytokines and matrix genes. mRNA stabilization and transcriptional up-regulation are involved in resistin-induced gene expression in human chondrocytes.

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“…Pathogenesis of RA involves cellular infiltration into the synovium and increase of inflammatory cytokines such as TNF-, IL-1 , and IL-6 consequently leading to cartilage and bone erosion (Arend, 2001;Choy and Panayi, 2001;Pratt et al, 2009;Choy, 2012). RASFs play critical role in the pathogenesis of RA by involvement in angiogenesis and in regulation of the inflammatory cells (Cawston, 1995;Han et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…IL-1 induces the proliferation of RASFs and also causes the production of high levels of inflammatory mediators-MMPs and prostaglandin E2 (PGE2) (Choy and Panayi, 2001). While the pathogenesis of RA is not completely understood, the process is reported to involve cellular infiltration into the synovial tissue with marked increase of inflammatory cytokinestumor necrosis factor(TNF) , interleukin(IL)-1 and IL-6, that eventually contribute to cartilage and bone erosion (Arend, 2001;Choy, 2012). These mediators activate major signalling pathways such as the nuclear factor (NF)-κB and mitogen activated protein kinases (MAPKs) (Tas et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Tangeretin inhibits IL-1β induced proliferation of rheumatoid synovial fibroblasts and the production of COX-2, PGE2 and MMPs via modulation of p38 MAPK/ERK/JNK pathways

Zhang

et al. 2015

Bangladesh J Pharmacol

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The study aimed to determine the effect of tangeretin in inhibiting the interleukin-1 (IL-1 )-induced proliferation of RASFs and suppression of the production of inflammatory mediators. RASFs were isolated from synovial tissue obtained from patients with RA during knee arthroscopy. The cells were exposed to IL-1 (1.0 ng/mL) and/ or tangeretin (50 or 100 µM). Cell viability was assessed following treatments. Expressions of MMPs and COX-2 were analysed by real-time PCR and western blotting. Production of prostaglandin E2 (PGE2) by RASFs were analysed by ELISA. Expressions of mitogen activated protein kinases (MAPKs) and nuclear factor-kB (NF-kB) were assessed by western blotting. Tangeretin significantly inhibited the proliferation of RASFs, as well as down-regulated the expression of MMP-1, MMP-3 and COX-2 mRNA and protein and also the phosphorylation of ERK, p38 and JNK. Raised level of expression of NF-κB and PGE2 induced by IL-1 was reduced by tangeretin. Results indicate that tangeretin was effective in inhibiting the synovial fibroblast proliferation, as well regulated MMPs, COX-2, PGE2 via modulation of p38 MAPK, ERK and JNK pathways. Article Info

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Cytokines and cellular interactions in inflammatory synovitis

Cited by 16 publications

References 21 publications

Concentration of the CS-846 Epitope in Serum and Synovial Fluid of Horses with Different Grades of Osteochondral Fragments in the Carpal Joints

Concentration of the CS-846 Epitope in Serum and Synovial Fluid of Horses with Different Grades of Osteochondral Fragments in the Carpal Joints

Resistin induces expression of proinflammatory cytokines and chemokines in human articular chondrocytes via transcription and messenger RNA stabilization

Tangeretin inhibits IL-1β induced proliferation of rheumatoid synovial fibroblasts and the production of COX-2, PGE2 and MMPs via modulation of p38 MAPK/ERK/JNK pathways

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