EFFECT OF INTERLEUKIN 1 AND LEUKAEMIA INHIBITORY FACTOR ON CHONDROCYTE METABOLISM IN ARTICULAR CARTILAGE FROM NORMAL AND INTERLEUKIN-6-DEFICIENT MICE: ROLE OF NITRIC OXIDE AND IL-6 IN THE SUPPRESSION OF PROTEOGLYCAN SYNTHESIS

Cytokine ◽  
1997 ◽  
Vol 9 (7) ◽  
pp. 453-462 ◽  
Author(s):  
Fons A.J. Van de Loo ◽  
Onno J. Arntz ◽  
Wim B. Van den Berg
Keyword(s):  
Nitric Oxide ◽  
Articular Cartilage ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
Inhibitory Factor ◽  
Leukaemia Inhibitory Factor ◽  
Proteoglycan Synthesis ◽  
Chondrocyte Metabolism ◽  
Deficient Mice

scholarly journals Regulation of matrix turnover in meniscal explants: role of mechanical stress, interleukin-1, and nitric oxide

2003 ◽  
Vol 95 (1) ◽  
pp. 308-313 ◽  
Author(s):  
Sang-jin Shin ◽  
Beverley Fermor ◽  
J. Brice Weinberg ◽  
David S. Pisetsky ◽  
Farshid Guilak
Keyword(s):  
Nitric Oxide ◽  
Mechanical Stress ◽  
Dynamic Compression ◽  
Interleukin 1 ◽  
Joint Disease ◽  
Proteoglycan Synthesis ◽  
Compressive Stresses ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

The meniscus is an intra-articular fibrocartilaginous structure that serves essential biomechanical roles in the knee. With injury or arthritis, the meniscus may be exposed to significant changes in its biochemical and biomechanical environments that likely contribute to the progression of joint disease. The goal of this study was to examine the influence of mechanical stress on matrix turnover in the meniscus in the presence of interleukin-1 (IL-1) and to determine the role of nitric oxide (NO) in these processes. Explants of porcine menisci were subjected to dynamic compressive stresses at 0.1 MPa for 24 h at 0.5 Hz with 1 ng/ml IL-1, and the synthesis of total protein, proteoglycan, and NO was measured. The effects of a nitric oxide synthase 2 (NOS2) inhibitor were determined. Dynamic compression significantly increased protein and proteoglycan synthesis by 68 and 58%, respectively, compared with uncompressed explants. This stimulatory effect of mechanical stress was prevented by the presence of IL-1 but was restored by specifically inhibiting NOS2. Release of proteoglycans into the medium was increased by IL-1 or mechanical compression and further enhanced by IL-1 and compression together. Stimulation of proteoglycan release in response to compression was dependent on NOS2 regardless of the presence of IL-1. These finding suggest that IL-1 may modulate the effects of mechanical stress on extracellular matrix turnover through a pathway that is dependent on NO.

scholarly journals Interleukin-1-induced interleukin-6 is required for the inhibition of proteoglycan synthesis by interleukin-1 in human articular cartilage

1990 ◽  
Vol 33 (11) ◽  
pp. 1695-1701 ◽  
Author(s):  
J. J. Nietfeld ◽  
B. Wilbrink ◽  
M. Helle ◽  
J. L. A. M. Van Roy ◽  
W. Den Otter ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
Proteoglycan Synthesis ◽  
Human Articular Cartilage

scholarly journals Role of nitric oxide in the inhibition of BMP-2-mediated stimulation of proteoglycan synthesis in articular cartilage

2000 ◽  
Vol 8 (2) ◽  
pp. 82-86 ◽  
Author(s):  
P.M. van der Kraan ◽  
E.L. Vitters ◽  
H.M. van Beuningen ◽  
F.A.J. van de Loo ◽  
W.B. van den Berg
Keyword(s):  
Nitric Oxide ◽  
Articular Cartilage ◽  
Proteoglycan Synthesis ◽  
Stimulation Of

The role of leukaemia inhibitory factor and interleukin-6 in human reproduction

1998 ◽  
Vol 13 (suppl 3) ◽  
pp. 237-243 ◽  
Author(s):  
S.K. Smith ◽  
D.S. Charnock-Jones ◽  
A.M. Sharkey
Keyword(s):  
Interleukin 6 ◽  
Inhibitory Factor ◽  
Human Reproduction ◽  
Leukaemia Inhibitory Factor

scholarly journals Role of interleukin-25 in development of spontaneous arthritis in interleukin-1 receptor antagonist-deficient mice

2017 ◽  
Vol 12 ◽  
pp. 62-65
Author(s):  
Yasuharu Abe ◽  
Aya Nambu ◽  
Sachiko Yamaguchi ◽  
Ayako Takamori ◽  
Hajime Suto ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Interleukin 1 Receptor Antagonist ◽  
Interleukin 25 ◽  
Deficient Mice

Selected Contribution: Differential role of nitric oxide synthase isoforms in fever of different etiologies: studies using Nosgene-deficient mice

2003 ◽  
Vol 94 (6) ◽  
pp. 2534-2544 ◽  
Author(s):  
Wieslaw Kozak ◽  
Anna Kozak
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Corn Oil ◽  
Normal Male ◽  
Wild Type ◽  
Oxide Synthase ◽  
And Control ◽  
Nos Isoforms ◽  
Deficient Mice

Male C57BL/6J mice deficient in nitric oxide synthase (NOS) genes (knockout) and control (wild-type) mice were implanted intra-abdominally with battery-operated miniature biotelemeters (model VMFH MiniMitter, Sunriver, OR) to monitor changes in body temperature. Intravenous injection of lipopolysaccharide (LPS; 50 μg/kg) was used to trigger fever in response to systemic inflammation in mice. To induce a febrile response to localized inflammation, the mice were injected subcutaneously with pure turpentine oil (30 μl/animal) into the left hindlimb. Oral administration (gavage) of N G-monomethyl-l-arginine (l-NMMA) for 3 days (80 mg · kg−1 · day−1in corn oil) before injection of pyrogens was used to inhibit all three NOSs ( N G-monomethyl-d-arginine acetate salt and corn oil were used as control). In normal male C57BL/6J mice, l-NMMA inhibited the LPS-induced fever by ∼60%, whereas it augmented fever by ∼65% in mice injected with turpentine. Challenging the respective NOS knockout mice with LPS and with l-NMMA revealed that inducible NOS and neuronal NOS isoforms are responsible for the induction of fever to LPS, whereas endothelial NOS (eNOS) is not involved. In contrast, none of the NOS isoforms appeared to trigger fever to turpentine. Inhibition of eNOS, however, exacerbates fever in mice treated with l-NMMA and turpentine, indicating that eNOS participates in the antipyretic mechanism. These data support the hypothesis that nitric oxide is a regulator of fever. Its action differs, however, depending on the pyrogen used and the NOS isoform.

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