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      Dynamic compression inhibits the synthesis of nitric oxide and PGE(2) by IL-1beta-stimulated chondrocytes cultured in agarose constructs.

      Biochemical and Biophysical Research Communications
      Animals, Cartilage, Articular, Cattle, Cell Culture Techniques, methods, Cells, Cultured, Chondrocytes, cytology, drug effects, physiology, Dinoprostone, biosynthesis, Interleukin-1, pharmacology, Models, Biological, Nitric Oxide, Nitrites, metabolism, Sepharose, Stress, Mechanical, Sulfates, Thymidine, Tritium, Weight-Bearing

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          Abstract

          Both mechanical loading and interleukin-1beta (IL-1beta) are known to regulate metabolic processes in articular cartilage through pathways mediated by nitric oxide ((*)NO) and PGE(2). This study uses a well-characterized model system involving isolated chondrocytes cultured in agarose constructs to test the hypothesis that dynamic compression alters the synthesis of (*)NO and PGE(2) by IL-1beta-stimulated articular chondrocytes. The data presented demonstrate for the first time that dynamic compression counteracts the effects of IL-1beta on articular chondrocytes by suppressing both (*)NO and PGE(2) synthesis. Inhibitor experiments indicated that the dynamic compression-induced inhibition of PGE(2) synthesis and stimulation of proteoglycan synthesis were (*)NO mediated, while compression-induced stimulation of cell proliferation was (*)NO independent. The inhibition of (*)NO and PGE(2) by dynamic compression is a finding of major significance that could contribute to the development of novel strategies for the treatment of cartilage-degenerative disorders. Copyright 2001 Academic Press.

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