Induction of the chemokine IL-8/Kc by the articular cartilage: Possible influence on osteoarthritis

Chauffier, Karine; Laiguillon, Marie-Charlotte; Bougault, Carole; Gosset, Marjolaine; Priam, Sabrina; Salvat, Colette; Mladenović, Z.; Nourissat, Geoffroy; Jacques, Claire; Houard, Xavier; Bérenbaum, Francis; Sellam, Jérémie

doi:10.1016/j.jbspin.2011.12.013

Cited by 61 publications

(41 citation statements)

References 37 publications

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“…Chondrocytes also express chemokine receptors including CXCR3, CXCR4, CXCR5, and CCR6 and chemokines including IL-8, macrophage inflammatory protein 1α, GROαβγ, monocyte chemotactic protein 1, and RANTES, which may play important roles in activating catabolic pathways and chondrocyte hypertrophy [Chauffier et al 2012;Loeser, 2011;Mazzetti et al 2004;Merz et al 2003;Sandell et al 2008]. Many chemokines are produced in joint tissues of patients with OA and after joint injury [Cuellar et al 2009;Endres et al 2010;Scanzello et al 2011].…”

Section: Inflammation and Mechanical Stress In Osteoarthritismentioning

confidence: 99%

Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis

Goldring

2012

Therapeutic Advances in Musculoskeletal

374

302

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Chondrogenesis occurs as a result of mesenchymal cell condensation and chondroprogenitor cell differentiation. Following chondrogenesis, the chondrocytes remain as resting cells to form the articular cartilage or undergo proliferation, terminal differentiation to chondrocyte hypertrophy, and apoptosis in a process termed endochondral ossification, whereby the hypertrophic cartilage is replaced by bone. Human adult articular cartilage is a complex tissue of matrix proteins that varies from superficial to deep layers and from loaded to unloaded zones. A major challenge to efforts to repair cartilage by stem cell-based and other tissue-engineering strategies is the inability of the resident chondrocytes to lay down a new matrix with the same properties as it had when it was formed during development. Thus, understanding and comparing the mechanisms of cartilage remodeling during development, osteoarthritis (OA), and aging may lead to more effective strategies for preventing cartilage damage and promoting repair. The pivotal proteinase that marks OA progression is matrix metalloproteinase 13 (MMP-13), the major type II collagen-degrading collagenase, which is regulated by both stress and inflammatory signals. We and other investigators have found that there are common mediators of these processes in human OA cartilage. We also observe temporal and spatial expression of these mediators in early through late stages of OA in mouse models and are analyzing the consequences of knockout or transgenic overexpression of critical genes. Since the chondrocytes in adult human cartilage are normally quiescent and maintain the matrix in a low turnover state, understanding how they undergo phenotypic modulation and promote matrix destruction and abnormal repair in OA may to lead to identification of critical targets for therapy to block cartilage damage and promote effective cartilage repair.

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Section: Inflammation and Mechanical Stress In Osteoarthritismentioning

confidence: 99%

Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis

Goldring

2012

Therapeutic Advances in Musculoskeletal

374

302

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“…Briefly, the cartilage explants were cut into small pieces (~5 mm 3 ), washed several times with phosphate buffered saline (PBS) and incubated in DMEM culture medium containing 25 mM glucose necessary for human explant maintenance, and supplemented with 100 U/mL penicillin, 100 mg/mL streptomycin, and 4 mM glutamine for 24 h at 37 C with or without IL-1b (5 ng/mL). Conditioned media (CM) were then collected, centrifuged (1600 g for 6 min) and stored at À20 C. Each volume of medium was normalized to wet weight of explants (6 mL/g tissue) 27 .…”

Section: Collection Of Oa Human Cartilagementioning

confidence: 99%

Characterization of diabetic osteoarthritic cartilage and role of high glucose environment on chondrocyte activation: toward pathophysiological delineation of diabetes mellitus-related osteoarthritis

Laiguillon

Courties

Houard

et al. 2015

Osteoarthritis and Cartilage

107

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“…Also in these cells, visfatin expression was necessary for IL-1β stimulated PGE2 production, which suggests a potential autocrine role for this adipokine in PGE2 synthesis [41]. Likewise, in murine chondrocytes, visfatin can regulate the expression/production of certain cytokines and catabolic factors such as the murine equivalent of IL-8, Kc [45], also been linked with impaired insulin sensitivity [15]. However, studies performed in RA patients have shown that serum visfatin levels do not correlate with insulin resistance [25,26,29] or with insulin resistance after inflammation adjustment [32].…”

Section: Visfatin In Rheumatoid Arthritis (Ra)mentioning

confidence: 89%

Visfatin: a new player in rheumatic diseases

Gómez

Suárez²,

Villalvilla³

et al. 2013

Immunometabolism

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During the last 50 years the number of overweight and obese people in developed countries has increased dramatically. The consequences of this excessive fat accumulation have been associated with a multitude of comorbidities, mainly related to the cardiovascular system and glucose and lipid metabolism. However, obesity also has an impact on other diseases, as an enhancer of certain pathological aspects or as a susceptibility factor, including certain rheumatic diseases such as rheumatoid arthritis (RA), osteoarthritis (OA) and systemic lupus erythematosus (SLE). The link between obesity and these rheumatic diseases has been purported to be via the action of metabolic factors produced by adipose tissue, adipokines. Among these adipokines are leptin and adiponectin, which have been extensively studied. Our knowledge of the role of other relevant newer adipokines, such as visfatin, in the arthritides is rapidly growing. Therefore, in this review our aim is to summarize the current literature regarding the association between visfatin and the most relevant rheumatic diseases.

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Induction of the chemokine IL-8/Kc by the articular cartilage: Possible influence on osteoarthritis

Cited by 61 publications

References 37 publications

Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis

Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis

Characterization of diabetic osteoarthritic cartilage and role of high glucose environment on chondrocyte activation: toward pathophysiological delineation of diabetes mellitus-related osteoarthritis

Visfatin: a new player in rheumatic diseases

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