Malondialdehyde oxidation of cartilage collagen by chondrocytes

Tiku, M. L.; Allison, Greg; Naik, Karishma; Karry, S.K

doi:10.1016/s1063-4584(02)00348-5

Cited by 53 publications

(29 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A series of antioxidants, such as vitamin C (Tiku et al 2003), vitamin E (Bhatti et al 2013), and sodium ferulate (Shang et al 2009), have been demonstrated their chondro-protective properties, as well as potentials in reducing apoptosis and senescence. Cartilage specific proteins including collagen type II and aggrecan can also be elevated after treatment with these agents (Bhatti et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Chondroprotective Effects of Taurine in Primary Cultures of Human Articular Chondrocytes

Liu

et al. 2015

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Articular cartilage is characterized by the lack of blood vessels and has a poor self-healing potential. Limited cell numbers and dedifferentiation of chondrocytes when expanded in vitro are the major obstacles of autologous chondrocyte implantation. Autologous chondrocyte implantation is a cell-based treatment that can be used as a second-line measure to regenerate chondral or osteochondral defects in younger, active patients. There is an urgent need to find an effective chondrogenic protection agent alleviating or inhibiting chondrocyte dedifferentiation. In this study, we explored the effect of taurine (2-aminoethane sulfonic acid) on proliferation and phenotype maintenance of human articular chondrocytes by analyzing the cell proliferation, morphology, viability, and expression of cartilage specific mRNAs and proteins. Primary chondrocytes were isolated from human articular cartilage tissues. Results showed that taurine effectively promoted chondrocyte growth and enhanced accumulation of glycosaminoglycans and collagens in the conditioned media of chondrocytes. Moreover, taurine exposure caused significant increases in the relative expression levels of mRNAs for cartilage specific markers, including aggrecan, collagen type II and SOX9. Aggrecan is a cartilage-specific proteoglycan, and SOX9 is a chondrogenic transcription factor. In contrast, the mRNA expression of collagen type I, a marker for chondrocyte dedifferentiation, was significantly decreased in cells treated with taurine, indicating that taurine inhibits the chondrocyte dedifferentiation. This study reveals that taurine is effective in proliferation promotion and phenotype maintenance of chondrocytes. Thus, taurine may be a useful pro-chondrogenic agent for autologous chondrocyte implantation in the treatment of cartilage repair.

show abstract

Section: Introductionmentioning

confidence: 99%

Chondroprotective Effects of Taurine in Primary Cultures of Human Articular Chondrocytes

Liu

et al. 2015

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

show abstract

“…Using this model, we showed that chondrocyte-derived lipid peroxidation mediates collagen degradation and that vitamin E inhibits this degradation process (28). More recently, we demonstrated that malondialdehyde (MDA), a toxic aldehydic end product of lipid peroxidation, mediates the oxidation of cartilage collagen (29). MDA and hydroxynonenal (HNE) are specific and major aldehydic products of lipid peroxidation that are believed to be largely responsible for the cytopathologic effects observed during the oxidative stress of lipid peroxidation (23,24).…”

mentioning

confidence: 99%

The presence of molecular markers of in vivo lipid peroxidation in osteoarthritic cartilage: A pathogenic role in osteoarthritis

Shah¹,

Raska²,

Tiku³

2005

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. To investigate the role of oxidative functions in human osteoarthritic (OA) chondrocytes and to investigate the presence of in vivo molecular markers of lipoxidation in OA cartilage.Methods. An in vitro model of cartilage collagen degradation was used. Lipid peroxidation activity and overall oxidative function in OA chondrocytes were monitored by cis-parinaric acid and dichlorofluorescein assays, respectively. In vivo molecular markers of lipoxidation in normal and OA cartilage were studied using immunohistochemistry to detect the presence of malondialdehyde and hydroxynonenal adducts.Results. Human OA chondrocytes showed a robust amount of 3 H-proline-labeled collagen degradation upon stimulation with lipopolysaccharide and calcium ionophore A21387, as compared with that in untreated OA chondrocytes. Primary OA chondrocytes showed both spontaneous and inducible levels of lipid peroxidation activity. However, lipid peroxidation activity was already maximally elevated in more than 50% of the OA chondrocyte samples. Overall, spontaneous and inducible oxidative activities were observed in all OA samples. Immunohistochemical analysis of control OA tissue sections that were not treated with monoclonal antibody showed little immunoreactivity. OA cartilage sections treated with monoclonal antibodies showed specific immunoreactivity on the cartilage surface, at sites of OA lesions, at the pericellular matrix, and at intra-and intercellular matrices. Normal cartilage sections showed faint surface reactivity.Conclusion. Our observations suggest that human OA chondrocytes demonstrate spontaneous and inducible cell-associated lipoxidative and nonlipoxidative activity. Lipoxidative activity appears to be enhanced in OA chondrocytes. The presence of molecular markers of in vivo lipid peroxidation was demonstrated in OA cartilage, suggesting its role in the pathogenesis of the disease.Osteoarthritis (OA) is the most common form of joint disease that affects humans. The incidence of OA increases during every decade of life, and by the age of 65 years, almost one-third of the population has OA of the knee joints. The economic burden attributed to the joint pain and disability of OA amounts to billions of dollars each year (1). As the population demographic in the US changes to a predominantly older generation, the increasing prevalence of OA will be a major public health problem.There is currently no treatment available that will prevent or cure OA. Pharmacologic and nonpharmacologic agents used for OA provide only symptomatic relief of pain. The lack of specific therapy for this disease is perhaps due to our limited understanding of its pathogenesis. Understanding the molecular mechanisms involved in the development of OA will help us to develop ways to prevent or reverse the degenerative process of the disease.Current concepts of the pathogenic mechanisms of OA suggest that there is a shift in the homeostatic balance between the destruction and synthesis of bone and cartilage, with a net progressive destruction of t...

show abstract

“…The unique distribution of lipids in cartilage, which changes significantly with age, and dietary intake of lipids could influence the lipid peroxidizability of cartilage. It is possible that alteration in lipid metabolism and oxidative stress could be a catalyst for cartilage aging (Tiku et al 2003). Age-related changes in the lipid composition of cartilage could push the normally contained lipid peroxidation process into a state of uncontrolled oxidative stress, leading to the oxidation of cartilage collagen.…”

Section: Discussionmentioning

confidence: 99%

The role of TAMMEF therapy on the antioxidant status in osteoarthritis

et al. 2009

View full text Add to dashboard Cite

Osteoarthritis (OA) is the most common joint disorder, associated with loss of articular cartilage, osteophyte formation, subchodral bone change, synovitis and characterized by chronic and often disabling pain and stiffness of one or more joints. The pathogenesis of the disease is complex and still debated, even if recent studies have shown that reactive oxygen species may participate in the initiation and progression of OA. Moreover, it is known that pulsed electromagnetic fields are useful in the OA treatment, owing to their analgesic and anti-inflammatory properties. This work evaluated lipid peroxidation, glutathione, and ascorbic acid levels in patients with OA of spine, before and after the application of a new electromagnetic system, the TAMMEF (Therapeutic Application of a Musically Modulated Electromagnetic Field) system. In TAMMEF system, the extremely low frequencies electromagnetic field is piloted by a musical signal and its parameters (frequency, intensity, waveform) are modified in time, randomly varying within the respective ranges: so all possible codes can occur during a single application. Twenty patients affected by OA of spine and 20 healthy subjects were enrolled in this study. Plasma levels of ascorbic acid (AA), glutathione (GSH) and malondialdehyde (MDA) (as index of lipid peroxidation) were determined in patients and controls, before the beginning of treatment (first day of therapy) and at the end of cycle. All patients underwent a cycle of 10 daily sessions of 30 min each. Our study showed a significant increase of MDA level and a significant decrease of both AA and GSH levels in patients with OA compared to control group. These findings support the role of oxidative stress in the pathogenesis of OA. After TAMMEF treatment in the OA group, analysis revealed a significant decrease in plasma MDA and AA levels (P \ 0.05 and P \ 0.01, respectively), no significant difference in GSH levels. Reduction in MDA level could be due to the decreased generation of reactive oxygen species and/or to the increased detoxification activity mediated by GSH. No significant difference in GSH levels, evidenced in OA patients after TAMMEF treatment, could be due to effect sparing of AA on GSH. Furthermore, a beneficial symptomatic effect was observed in all patients.

show abstract

Malondialdehyde oxidation of cartilage collagen by chondrocytes

Cited by 53 publications

References 39 publications

Chondroprotective Effects of Taurine in Primary Cultures of Human Articular Chondrocytes

Chondroprotective Effects of Taurine in Primary Cultures of Human Articular Chondrocytes

The presence of molecular markers of in vivo lipid peroxidation in osteoarthritic cartilage: A pathogenic role in osteoarthritis

The role of TAMMEF therapy on the antioxidant status in osteoarthritis

Contact Info

Product

Resources

About