Abstract
Chemerin is a chemokine that, through the engagement of its counter-receptor, ChemR23, attracts pro-inflammatory cells. However, chemerin has been shown to play other functions and a recent study by Berg and colleagues demonstrates that chemerin/ChemR23 is a system beyond chemokines. Human articular chondrocytes produce chemerin and express ChemR23, and upon stimulation with recombinant chemerin increase the production of pro-catabolic cytokines and metalloproteinases. The latter are up-regulated in osteoarthritic cartilage and cause extracellular matrix breakdown. Since an increase of chemerin in fat tissue and serum of obese patients has been reported, this new feature of chemerin may represent a functional link between obesity and osteoarthritis.
Highlights
Chemerin is a chemokine that, through the engagement of its counter-receptor, ChemR23, attracts pro-inflammatory cells
A series of experiments was performed on human native cartilage or cultured chondrocytes isolated from joints of patients undergoing knee arthroplasty for severe OA, and patients subjected to autologous chondrocyte transplantation
ChemR23 and chemerin proteins were detected in chondrocytes in vitro by immunocytochemistry
Summary
Chemerin is a chemokine that, through the engagement of its counter-receptor, ChemR23, attracts pro-inflammatory cells. Knowledge of the pathophysiology of articular cartilage is crucial in understanding the mechanisms underlying joint diseases such as osteoarthritis (OA) and rheumatoid arthritis (RA). In a previous issue of Arthritis Research and Therapy, Berg and colleagues [1] have provided new insights in this field by showing for the first time that chondrocytes express chemerin and its cognate receptor, ChemR23, and that this system may be involved in cartilage degradation.
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