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.

Nitric oxide inhibits chondrocyte response to IGF-I: inhibition of IGF-IRβ tyrosine phosphorylation

2000 ◽  
Vol 279 (4) ◽  
pp. C961-C969 ◽  
Author(s):  
R. K. Studer ◽  
E. Levicoff ◽  
H. Georgescu ◽  
L. Miller ◽  
D. Jaffurs ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interleukin 1 ◽  
Proteoglycan Synthesis ◽  
Igf I ◽  
Adenoviral Transfer ◽  
Inos Knockout Mice ◽  
Oxide Synthase ◽  
The Relationship ◽  
Deta Nonoate

Chondrocytes in arthritic cartilage respond poorly to insulin-like growth factor I (IGF-I). Studies with inducible nitric oxide synthase (iNOS) knockout mice suggest that NO is responsible for part of the cartilage insensitivity to IGF-I. These studies characterize the relationship between NO and chondrocyte responses to IGF-I in vitro, and define a mechanism by which NO decreases IGF-I stimulation of chondrocyte proteoglycan synthesis. Lapine cartilage slices, chondrocytes, and cartilage from osteoarthritic (OA) human knees were exposed to NO from the donors S-nitroso- N-acetylpenicillamine (SNAP) or ( Z)-1-[2-(2-aminoethyl)- N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate] (DETA NONOate), by transduction with adenoviral transfer of iNOS (Ad-iNOS), or by activation with interleukin-1 (IL-1). NO synthesis was estimated from medium nitrite, and proteoglycan synthesis was measured as incorporation of 35SO4. IGF-I receptor phosphorylation was evaluated with Western analysis. SNAP, DETA NONOate, endogenously synthesized NO in Ad-iNOS-transduced cells, or IL-1 activation decreased IGF-I-stimulated proteoglycan synthesis in cartilage and monolayer cultures of chondrocytes. OA cartilage responded poorly to IGF-I; however, the response to IGF-I was restored by culture with N G-monomethyl-l-arginine(l-NMA). IGF-I receptor phosphotyrosine was diminished in chondrocytes exposed to NO. These studies show that NO is responsible for part of arthritic cartilage/chondrocyte insensitivity to anabolic actions of IGF-I; inhibition of receptor autophosphorylation is potentially responsible for this effect.

scholarly journals Knockdown of TRIM8 Attenuates IL-1β-induced Inflammatory Response in Osteoarthritis Chondrocytes Through the Inactivation of NF-κB Pathway

2020 ◽  
Vol 29 ◽  
pp. 096368972094360
Author(s):  
Ruoxi Liu ◽  
Hao Wu ◽  
Huanjin Song
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Interleukin 1 ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Prostaglandin E ◽  
Tnf Α ◽  
Osteoarthritis Chondrocytes ◽  
Oa Chondrocytes ◽  
Oxide Synthase

Osteoarthritis (OA) is a degenerative joint disease associated with inflammatory response. Tripartite motif 8 (TRIM8) is a member of TRIM family that has been found to regulate inflammation. The present study was aimed to evaluate the role of TRIM8 in OA chondrocytes. Our results showed that TRIM8 expression was significantly increased in interleukin 1 beta (IL-1β)-stimulated OA chondrocytes. To knock down the TRIM8 expression in chondrocytes, the chondrocytes were transfected with si-TRIM8. Knockdown of TRIM8 attenuated IL-1β-induced production of inflammatory mediators including nitric oxide and prostaglandin E2. The increased expression levels of inducible nitric oxide synthase and cyclooxygenase-2 in IL-1β-induced chondrocytes were suppressed by TRIM8 knockdown. The IL-1β-induced production of proinflammatory cytokines including TNF-α and IL-6 was significantly decreased after transfection with si-TRIM8. Besides, knockdown of TRIM8 mitigated the IL-1β-induced decrease in aggrecan and collagen-II proteins expression and increase in matrix-degrading enzymes in chondrocytes. Furthermore, TRIM8 knockdown prevented IL-1β-induced nuclear factor kappa B (NF-κB) activation in chondrocytes. Taken together, these findings indicated that knockdown of TRIM8 attenuates IL-1β-induced inflammatory response in OA chondrocytes through the inactivation of NF-κB pathway. Thus, targeting TRIM8 might provide therapeutic treatment for OA.

Role of nitric oxide synthesized by nitric oxide synthase 2 in liver regeneration

2008 ◽  
Vol 28 (6) ◽  
pp. 865-877 ◽  
Author(s):  
Takafumi Kumamoto ◽  
Shinji Togo ◽  
Atsushi Ishibe ◽  
Daisuke Morioka ◽  
Kazuteru Watanabe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Liver Regeneration ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

Resveratrol attenuates lipopolysaccharide-induced hepatitis in d-galactosamine sensitized rats: Role of nitric oxide synthase 2 and heme oxygenase-1

Nitric Oxide ◽  
2009 ◽  
Vol 21 (3-4) ◽  
pp. 216-225 ◽  
Author(s):  
Hassan Farghali ◽  
Dalibor Černý ◽  
Ludmila Kameníková ◽  
Jindřich Martínek ◽  
Aleš Hořínek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase
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