Nitric oxide mediates suppression of cartilage proteoglycan synthesis by interleukin-1

D. Taskiran, M. Stefanic-Racic, H. Georgescu, Christopher H Evans

Research output: Contribution to journalArticle

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Abstract

Slices of rabbit articular cartilage synthesized large quantities of nitric oxide (NO) following exposure to human recombinant interleukin-1β (hrIL-1β) or rabbit synovial cytokines (CAF). Each of these stimuli also strongly suppressed the biosynthetic incorporation of 35S042- into the glycosaminoglycans (GAGs) of cartilage proteoglycans. Treatment of cartilage fragments with L-N(G)-monomethylarginine (L-NMA), a competitive inhibitor of NO synthase, both inhibited NO synthesis in response to IL-1 and CAF and restored proteoglycan synthesis. D-NMA was inactive in this regard, and L-arginine reversed the effects of L-NMA. S-nitrosylacetylpenicillamine (SNAP), an organic donor of NO, reversibly mimicked the effect of IL-1 and CAF on 35SO42- incorporation. These data suggest that endogenously synthesized NO is the mediator which reduces cartilage proteoglycan synthesis in response to cytokines such as IL-1 and CAF. Antagonists of NO production may promote cartilage matrix synthesis and thus have potential as chondroprotective or chondroreparative agents.

Original languageEnglish (US)
Pages (from-to)142-148
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume200
Issue number1
DOIs
StatePublished - 1994
Externally publishedYes

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Cartilage
Proteoglycans
Interleukin-1
Nitric Oxide
omega-N-Methylarginine
S-Nitroso-N-Acetylpenicillamine
Cytokines
Rabbits
Nitric Oxide Donors
Articular Cartilage
Glycosaminoglycans
Nitric Oxide Synthase
Arginine

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Nitric oxide mediates suppression of cartilage proteoglycan synthesis by interleukin-1. / Taskiran, D.; Stefanic-Racic, M.; Georgescu, H.; Evans, Christopher H.

In: Biochemical and Biophysical Research Communications, Vol. 200, No. 1, 1994, p. 142-148.

Research output: Contribution to journalArticle

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