Abstract
Incubation of rabbit articular chondrocytes with interleukin-1 beta caused time-dependent expression of NO synthase, determined as nitrite, after a lag period of 6h. The synthesis of nitrite was concentration-dependent and was inhibited by cycloheximide and NG-monomethyl-L-arginine, but not by dexamethasone or hydrocortisone. The synthesis of NO in the 100,000g supernatant of activated chondrocytes was inhibited by EGTA, but not by the calmodulin inhibitors W-13 or trifluoperazine. The synthesis of NO was half-maximal at approximately 20nM free Ca2+. Endotoxin also induced the expression of this NO synthase. Thus, rabbit articular chondrocytes express a novel inducible NO synthase which is Ca(2+)-dependent, and whose induction is not prevented by glucocorticoids.
MeSH terms
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Amino Acid Oxidoreductases / biosynthesis*
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Amino Acid Oxidoreductases / metabolism
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Animals
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Arginine / analogs & derivatives
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Arginine / pharmacology
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Calcium / pharmacology
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Calmodulin / antagonists & inhibitors
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Cartilage, Articular / drug effects
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Cartilage, Articular / enzymology*
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Cells, Cultured
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Cycloheximide / pharmacology
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Dexamethasone / pharmacology*
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Egtazic Acid / pharmacology
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Enzyme Induction
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Hydrocortisone / pharmacology*
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Indomethacin / pharmacology
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Interleukin-1 / pharmacology
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Kinetics
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Male
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Nitric Oxide Synthase
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Rabbits
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Sulfonamides / pharmacology
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Trifluoperazine / pharmacology
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omega-N-Methylarginine
Substances
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Calmodulin
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Interleukin-1
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Sulfonamides
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Trifluoperazine
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omega-N-Methylarginine
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Egtazic Acid
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Dexamethasone
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N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide
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Arginine
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Cycloheximide
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Nitric Oxide Synthase
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Amino Acid Oxidoreductases
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Calcium
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Hydrocortisone
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Indomethacin