Comparative effects of IL-1β and hydrogen peroxide (H2O2) on catabolic and anabolic gene expression in juvenile bovine chondrocytes

Martin, Grégoire; Andriamanalijaona, Rina; Mathy-Hartert, M.; Henrotin, Yves; Pujol, Jean-Pierre

doi:10.1016/j.joca.2005.03.009

Cited by 36 publications

(31 citation statements)

References 51 publications

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“…22 Treatment of chondrocytes with 50-100 μM H 2 O 2 for one day was reported to induce the transcription factor activator protein 1 and to up-regulate matrix metalloproteinase 3 expression. 23 We showed the up-regulated metalloproteinase mechanism for ADAMTS9 expression at a higher concentration of H 2 O 2 in this study.…”

supporting

confidence: 59%

Hydrogen Peroxide-Induced Oxidative Damage in Human Chondrocytes: The Prophylactic Effects of Hypericum Perforatum Linn Extract on Deoxyribonucleic acid Damage, Apoptosis and Matrix Remodeling by a Disintegrin-Like and Metalloproteinase With Thrombospondin Motifs Proteinases

et al. 2014

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Objectives: This in vitro study aimed to examine the protective roles of Hypericum perforatum Linn (HPL) extract on cell viability, DNA damage, apoptosis and a disintegrin-like and metalloproteinase with thrombospondin motifs (ADAMTS) proteins in chondrocytes induced by hydrogen peroxide (H2O2), as a model of chondrocytes subjected to reactive oxygen species (ROS) attack in rheumatoid arthritis and osteoarthritis. Materials and methods: Human chondrosarcoma cell line (OUMS-27) was used. Cells were incubated with different concentrations of methanolic extract (100, 400, and 750 μg/ml) of HPL for 36 hours, and then treated with 0.7 mM H2O2 for two hours. Trypan blue was used for evaluation of cell viability, while DNA damage was evaluated by alkaline Comet assay. Caspase-1, ADAMTS5, ADAMTS9, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) proteins were analyzed by Western blot. Results: In vitro H2O2 treatment decreased OUMS-27 cell viability. Cells pretreated with HPL at concentration of 400 μg/mL were best protected from H2O2 toxicity. Compared to 100 μg/ml concentration, pretreatment of cells with 750 or 400 μg/ml of HPL generated more protection against H2O2-induced DNA damage. Hydrogen peroxide application to the cells led to a slight increase in Caspase-1 expression, which shows no apoptosis. The most prominent increase in Caspase-1 level was shown in cells treated with 400 μg/ml of HPL extract. There was an increase in ADAMTS9 and a decrease in ADAMTS5 levels upon H2O2 administration. Pretreatment with HPL led to more decrease in ADAMTS5 level, indicating the protection of extracellular matrix attacked by these proteinases in cartilage tissue. Conclusion: It can be concluded that HPL has a potential to reverse the negative effects and processes induced by H2O2 in OUMS-27 cells and it can protect the surrounding cartilage area of chondrocytes from oxidative damage, which is suggested to be one of the main molecular factors accused for progression of rheumatoid arthritis and osteoarthritis.

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supporting

confidence: 59%

Hydrogen Peroxide-Induced Oxidative Damage in Human Chondrocytes: The Prophylactic Effects of Hypericum Perforatum Linn Extract on Deoxyribonucleic acid Damage, Apoptosis and Matrix Remodeling by a Disintegrin-Like and Metalloproteinase With Thrombospondin Motifs Proteinases

et al. 2014

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“…It has been also demonstrated that IL-1b and hydrogen peroxide caused the activation of the redox-dependent transcription of NF-κB and AP-1 in bovine chondrocytes [45]. This effect triggers a remarkable decrease in type II collagen transcription, associated with a significant increase in MMP synthesis [45], leading to the onset of cartilage structural damage.…”

Section: Discussionmentioning

confidence: 95%

“…This effect triggers a remarkable decrease in type II collagen transcription, associated with a significant increase in MMP synthesis [45], leading to the onset of cartilage structural damage. Moreover, Terkeltaub et al [46] showed that IL-1β and TNFα induced the expression of important metalloproteinases, such as MMP-3 and MMP-13.…”

Section: Discussionmentioning

confidence: 99%

Butyrate Modulates Inflammation in Chondrocytes via GPR43 Receptor

Pirozzi

Francisco

Guida

et al. 2018

Cell Physiol Biochem

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Background/Aims: Osteoarthritis (OA) is a joint degenerative biomechanical disorder involving immunity, metabolic alterations, inflammation, and cartilage degradation, where chondrocytes play a pivotal role. OA has not effective pharmacological treatments and new therapeutic targets are needed. Adipokines contribute to the low-grade systemic inflammation in OA. Here, we explored novel molecular mechanisms of sodium butyrate (BuNa) in modulating inflammation and chemotaxis in chondrocytes, demonstrating the direct involvement of its G protein-coupled receptor (GPR)-43. Methods: ATDC5 murine chondrocytes were stimulated with interleukin (IL)-1β, in the presence or not of BuNa, for 24 h. RT-PCR and Western blot analysis was performed to evaluate the expression of inflammatory mediators and structural proteins. Results: Butyrate reduced the expression of canonic pro-inflammatory mediators (Nos2, COX-2, IL-6), pro-inflammatory adipokines (lipocalin-2 and nesfatin-1) and adhesion molecule (VCAM-1 and ICAM-1) in IL-1β-stimulated chondrocytes, inhibiting several inflammatory signalling pathways (NFκB, MAPKinase, AMPK-α, PI3K/Akt). Butyrate also reduced metalloproteinase production and limited the loss of type II collagen in IL-1β-inflamed chondrocytes. The chemoattractant effect of butyrate, after different inflammatory challenges, was revealed by increased annexin (AnxA)1 levels and chemokines expression. The chemoattractant and anti-inflammatory activities of butyrate were completely blunted by GPR43 silencing using RNA interference. Conclusion: Taken together, our data suggest the potential application of sodium butyrate as a novel candidate in a multi-target approach for the treatment of chondrocyte inflammation and cartilage degenerative process.

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“…At low concentrations, reactive oxygen species downregulate chondrocyte responses to proinflammatory cytokines 39 . However, at higher concentrations, reactive oxygen species directly damage the cartilage extracellular matrix, activate matrix metalloproteinases, suppress extracellular matrix synthesis, and induce matrix metalloproteinase expression through activation of the transcription factors activator protein 1 and nuclear factor kappaB 37,40,41 . In addition, concomitant exposure to nitric oxide and to the superoxide radical contributes to chondrocyte apoptosis 18,37 .…”

Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Inhibits Post-Impact Chondrocyte Death in Osteochondral Explants

Martin¹,

McCabe²,

Walter³

et al. 2009

The Journal of Bone and Joint Surgery-American Volume

124

166

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Comparative effects of IL-1β and hydrogen peroxide (H2O2) on catabolic and anabolic gene expression in juvenile bovine chondrocytes

Cited by 36 publications

References 51 publications

Hydrogen Peroxide-Induced Oxidative Damage in Human Chondrocytes: The Prophylactic Effects of Hypericum Perforatum Linn Extract on Deoxyribonucleic acid Damage, Apoptosis and Matrix Remodeling by a Disintegrin-Like and Metalloproteinase With Thrombospondin Motifs Proteinases

Hydrogen Peroxide-Induced Oxidative Damage in Human Chondrocytes: The Prophylactic Effects of Hypericum Perforatum Linn Extract on Deoxyribonucleic acid Damage, Apoptosis and Matrix Remodeling by a Disintegrin-Like and Metalloproteinase With Thrombospondin Motifs Proteinases

Butyrate Modulates Inflammation in Chondrocytes via GPR43 Receptor

N-Acetylcysteine Inhibits Post-Impact Chondrocyte Death in Osteochondral Explants

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