Hydrogen peroxide induces apoptosis of chondrocytes; involvement of calcium ion and extracellular signal-regulated protein kinase

Asada, Shigeki; Fukuda, Kanji; Nishisaka, Fumiaki; Matsukawa, M.; Hamanisi, C

doi:10.1007/s000110050719

Cited by 86 publications

(74 citation statements)

References 25 publications

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“…Results of our study demonstrated that, contrary to previous studies, H 2 O 2 may not induce chondrocyte apoptosis through caspase activation. 10,11 The secondary aim of the study was to evaluate the putative protective effect(s) of HPL extract against H 2 O 2 -induced alterations in apoptosis rate as well as the differences in aggrecan degradation in OUMS-27 cells using a viability test, comet assay, Caspase-1, and ADAMTS enzymes. Chondrocytes were pretreated with HPL extract and incubated with H 2 O 2 .…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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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“…Increased ROS production is considered to be an important cause of chondrocyte dysfunction and articular cartilage degradation, which leads to the pathogenesis of OA and the aging of cartilage (7)(8)(9)(10). Chondrocytes and cartilage tissues exhibit efficient protective strategies to minimize damage induced by increased ROS production, including H 2 O 2 (7,11). Previous studies have investigated various antioxidant supplements, including resveratrol, quercetin, vitamin E, and other strategies (12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Ascorbic acid provides protection for human chondrocytes against oxidative stress

Chang

Huo

et al. 2015

Molecular Medicine Reports

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Abstract. Oxidative stress is considered to be an important cause of dysfunction in chondrocytes and articular cartilage degradation, which leads to the pathogenesis of osteoarthritis (OA) and cartilage aging. The present study aimed to assess the effects of the widely applied antioxidant, ascorbic acid (AA), on human chondrocytes against hydrogen peroxide (H 2 O 2 ) in vitro. Using annexin V-fluorescein isothiocyanate, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and senescence-associated β-galactosidase assays, the present study identified that AA reduced apoptosis, reduced the loss of viability and markedly decreased H 2 O 2 -mediated senescence in cells treated with H 2 O 2 . Furthermore, AA not only stimulated the expression levels of collagens and proteoglycans, but also inhibited the differentiation of chondrocytes under conditions of oxidative stress. In addition, reverse transcription-quantitative polymerase chain reaction and western blotting demonstrated that AA decreased the activity of nrf2, NF-κB, AP1 and matrix metalloproteinase-3, which is stimulated by H 2 O 2 . In conclusion, AA efficiently protected human chondrocytes against damage induced by H 2 O 2 by regulating multiple regulatory pathways.

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“…Investigators in our group have previously demonstrated that ROS are involved in cartilage degradation associated with inflammatory joint disease (1)(2)(3)(4).…”

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confidence: 99%

Cyclic tensile stretch loaded on bovine chondrocytes causes depolymerization of hyaluronan: Involvement of reactive oxygen species

Yamazaki¹,

Fukuda²,

Matsukawa³

et al. 2003

Arthritis & Rheumatism

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Objective. We have previously demonstrated that reactive oxygen species (ROS) are involved in cartilage degradation. Decreased size of hyaluronan (HA), the major macromolecule in synovial fluid, to which it imparts viscosity, is reported in patients with arthritis. The purpose of this study was to determine the alteration in the molecular weight range of HA as a result of mechanical deformation loaded on the chondrocytes, as well as the involvement of ROS in this action.Methods. ROS were generated via the oxidation of hypoxanthine by xanthine oxidase. Cyclic tensile stretch was loaded using a vacuum-operated instrument. Levels of HA were measured using a sandwich enzyme-binding assay. Superoxide dismutase (SOD) activity and ROS were measured using water-soluble tetrazolium and a chemiluminescent probe, respectively.Results. ROS depolymerized HA molecules. Cyclic tensile stretch depolymerized HA and induced ROS. SOD inhibited not only ROS induction but also HA depolymerization caused by the mechanical stress.Conclusion. ROS play an important role in mechanical stress-induced HA depolymerization.

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Hydrogen peroxide induces apoptosis of chondrocytes; involvement of calcium ion and extracellular signal-regulated protein kinase

Abstract: Hydrogen peroxide induces chondrocyte apoptosis via Ca2+ signaling, and ERK is involved in these signal transduction pathways.

Cited by 86 publications

References 25 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

Ascorbic acid provides protection for human chondrocytes against oxidative stress

Cyclic tensile stretch loaded on bovine chondrocytes causes depolymerization of hyaluronan: Involvement of reactive oxygen species

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