The role of reactive oxygen species in homeostasis and degradation of cartilage

Henrotin, Yves; Brückner, Peter; Pujol, Jean-Pierre

doi:10.1016/s1063-4584(03)00150-x

Cited by 660 publications

(525 citation statements)

References 70 publications

Supporting

Mentioning

495

Contrasting

Unclassified

Order By: Relevance

“…This result could provide evidence of an increased extracellular matrix protein nitration in equine osteochondral lesions, since until recently, nitrotyrosine (NO (2) Tyr) formation has been considered to be a specific marker for protein oxidation by peroxynitrite (ONOO -), an unstable oxidant formed during neardiffusion limited interaction of superoxide ( ) and nitric oxide ) (Baldus et al, 2002;Brennan et al, 2002). Superoxide anion and nitric oxide productions in chondrocyte and in synovial cultures have been widely demonstrated (Stichtenoth and Frölich, 1998;Henrotin et al, 2003). However, in recent years other pathways of nitrotyrosine-formation have been suggested.…”

Section: Discussionmentioning

confidence: 99%

A type II-collagen derived peptide and its nitrated form as new markers of inflammation and cartilage degradation in equine osteochondral lesions

Gangl

Serteyn

Lejeune³

et al. 2007

Research in Veterinary Science

View full text Add to dashboard Cite

Markers of cartilage breakdown enable studying the degradation of cartilage matrix in equine joint pathologies. This study was designed to determine the levels of Coll2-1, a peptide of the triple helix of type II collagen, and Coll2-1NO 2 , its nitrated form in the plasma of healthy horses (controls; n = 37) and horses suffering from osteochondrosis (n = 34). Clinical and arthroscopic scores were attributed reflecting the severity of lesions and were related to the plasma levels of Coll2-1 and Coll2-1NO 2 . The median of Coll2-1 was significantly higher in the control group, whereas the mean of Coll2-1NO 2 showed significant elevation in the pathological group. However, the measurement means of scoring classes did not vary significantly. The markers were able to differentiate the group of horses suffering from osteochondrosis from the group of healthy horses. The elevation of Coll2-1NO 2 in the pathological group indicates an inflammation, mediated through reactive oxygen species and/or increased myeloperoxidase activity.

show abstract

Section: Discussionmentioning

confidence: 99%

A type II-collagen derived peptide and its nitrated form as new markers of inflammation and cartilage degradation in equine osteochondral lesions

Gangl

Serteyn

Lejeune³

et al. 2007

Research in Veterinary Science

View full text Add to dashboard Cite

show abstract

“…In these conditions, high levels of pro-inflammatory cytokines such as interleukin(IL)-1have been found in synovial fluids and may participate in collagen and proteoglycan degradation [1,2]. Moreover, chondrocyte activation by proinflammatory cytokines has been implicated in joint destruction through the production of catabolic enzymes and inflammatory mediators such as reactive oxygen species (ROS) and prostaglandin E 2 (PGE 2 ) [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…ROS can modulate cell signaling and exert damaging effects on cartilage as a consecuence of extracellular matrix degradation or chondrocyte apoptosis [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Heme oxygenase-1 induction modulates microsomal prostaglandin E synthase-1 expression and prostaglandin E2 production in osteoarthritic chondrocytes

Megías

Guillén²,

Clérigues³

et al. 2009

Biochemical Pharmacology

View full text Add to dashboard Cite

show abstract

“…Recent reports also revealed that chondrocyte aging is closely involved in oxidative stress, such as the induction of ROS by extrinsic stress (e.g., mechanical force) in degenerated articular cartilage (11)(12)(13)19,23). It has been reported that oxygen-derived free radicals directly damage the guanine repeats in the telomere DNA (24)(25)(26)(27).…”

mentioning

confidence: 99%

Water‐soluble C60 fullerene prevents degeneration of articular cartilage in osteoarthritis via down‐regulation of chondrocyte catabolic activity and inhibition of cartilage degeneration during disease development

Yudoh

Shishido

Murayama

et al. 2007

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. Studies have shown the roles of oxidative stress in the pathogenesis of osteoarthritis (OA) and induction of chondrocyte senescence during OA progression. The aim of this study was to examine the potential of a strong free-radical scavenger, watersoluble fullerene (C60), as a protective agent against catabolic stress-induced degeneration of articular cartilage in OA, both in vitro and in vivo.Methods. In the presence or absence of C60 (100 M), human chondrocytes were incubated with interleukin-1␤ (10 ng/ml) or H 2 O 2 (100 M), and chondrocyte activity was analyzed. An animal model of OA was produced in rabbits by resection of the medial meniscus and medial collateral ligament. Rabbits were divided into 5 subgroups: sham operation or treatment with C60 at 0.1 M, 1 M, 10 M, or 40 M. The left knee joint was injected intraarticularly with watersoluble C60 (2 ml), while, as a control, the right knee joint received 50% polyethylene glycol (2 ml), once weekly for 4 weeks or 8 weeks. Knee bone and cartilage tissue were prepared for histologic analysis. In addition, in the OA rabbit model, the effect of C60 (10 M) on degeneration of articular cartilage was compared with that of sodium hyaluronate (HA) (5 mg/ml).Results. C60 (100 M) inhibited the catabolic stress-induced production of matrix-degrading enzymes (matrix metalloproteinases 1, 3, and 13), downregulation of matrix production, and apoptosis and premature senescence in human chondrocytes in vitro.In rabbits with OA, treatment with water-soluble C60 significantly reduced articular cartilage degeneration, whereas control knee joints showed progression of cartilage degeneration with time. This inhibitory effect was dose dependent, and was superior to that of HA. Combined treatment with C60 and HA yielded a significant reduction in cartilage degeneration compared with either treatment alone. Conclusion.The results indicate that C60 fullerene is a potential therapeutic agent for the protection of articular cartilage against progression of OA.During the development of osteoarthritis (OA), mechanical and chemical stresses on articular cartilage change the stable cellular activities of chondrocytes and stimulate the production of growth factors and matrix proteins as well as inflammation mediators (1-4). It is well known that catabolic-stressed chondrocytes produce excess amounts of reactive oxygen species (ROS) (superoxide, nitric oxide, hydrogen peroxide, and peroxynitrite) as well as proinflammatory cytokines and chemokines (4-9).Studies have provided ample confirmation of the generation of ROS and the depletion of cellular antioxidants in degenerated articular cartilage (8-10). Numerous reports have indicated that the degeneration of articular cartilage is partially mediated by oxygenderived free radicals (8-12). Kurz et al reported that the extent of mechanical stress on articular cartilage is sufficient to stimulate an excess production of ROS from chondrocytes, leading to depolymerization of hyaluronic acid and chondrocyte death (11,12). Similarly, Gree...

show abstract

The role of reactive oxygen species in homeostasis and degradation of cartilage

Cited by 660 publications

References 70 publications

A type II-collagen derived peptide and its nitrated form as new markers of inflammation and cartilage degradation in equine osteochondral lesions

A type II-collagen derived peptide and its nitrated form as new markers of inflammation and cartilage degradation in equine osteochondral lesions

Heme oxygenase-1 induction modulates microsomal prostaglandin E synthase-1 expression and prostaglandin E2 production in osteoarthritic chondrocytes

Water‐soluble C60 fullerene prevents degeneration of articular cartilage in osteoarthritis via down‐regulation of chondrocyte catabolic activity and inhibition of cartilage degeneration during disease development

Contact Info

Product

Resources

About