Oxidative Stress Induces DNA Fragmentation and Caspase Activation Via the c-Jun NH2-terminal Kinase Pathway in H9c2 Cardiac Muscle Cells

Turner, Neil A.; Xia, Fang; Azhar, Gohar; Zhang, Xiaomin; Liu, Lixin; Wei, Jeanne Y.

doi:10.1006/jmcc.1998.0743

Cited by 180 publications

(112 citation statements)

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“…Recently, some reports demonstrated that H 2 O 2 was over produced in the pathological processes of myocardial death. Turner et al suggested that oxidative stress could result in the death of myocardial cells and activation of MAP kinase in H9c2 cells (Turner et al, 1998). Similar to our results, they showed that H 2 O 2 significantly decreased the viability of H9c2 cells.…”

Section: Discussionsupporting

confidence: 82%

The water extract of Omija protects H9c2 cardiomyoblast cells from hydrogen peroxide through prevention of mitochondrial dysfunction and activation of caspases pathway

Park

Shin

et al. 2006

Phytotherapy Research

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Section: Discussionsupporting

confidence: 82%

The water extract of Omija protects H9c2 cardiomyoblast cells from hydrogen peroxide through prevention of mitochondrial dysfunction and activation of caspases pathway

Park

Shin

et al. 2006

Phytotherapy Research

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“…It has been shown in cardiac muscle cells 56,57 and in brain neurons 58 that hypoxia-reoxygenation induced JNK 1 /SAPK 1 activation, which was involved in the apoptosis process. Very recently, Tournier et al 29 have shown that in the absence of JNK, UV-irradiated fibroblasts mitochondria did not release cytochrome c and did not start the apoptosis program, suggesting that JNK was mandatory for initiating programmed cell death, however, JNK 1 /SAPK 1 involvement in hypoxiareoxygenation induced apoptosis has not yet been proven in the liver.…”

Section: Discussionmentioning

confidence: 99%

Protein Kinase Activation by Warm And Cold Hypoxia- Reoxygenation in Primary-Cultured Rat Hepatocytes–JNK1/SAPK1 Involvement in Apoptosis

et al. 2000

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Ischemia-reperfusion procedures induced severe hepatic damages owing to different processes related to hypoxia and reoxygenation (H/R) phases, including the consecutive oxygen free radical (OFR) release. Stress-activated protein kinases (SAPKs) could be activated by extracellular stimuli. The aim of this study was to show whether H/R stress conditions could stimulate these kinases, and especially c-jun-N-terminal kinase (JNK 1 /SAPK 1 ), to reveal a potential role of JNK 1 /SAPK 1 in the control of hepatocyte apoptosis. Primary cultured rat hepatocytes, isolated from other liver cells and blood flow, were subjected to warm and cold hypoxiareoxygenation phases mimicking surgical and transplant conditions. The activation status of SAPKs was evaluated by immunoprecipitation or Western-blotting experiments, whereas apoptosis was assessed by measuring caspase activation and internucleosomal DNA fragmentation in vitro and by TUNEL reaction, in vivo. Hypoxia, and especially hypoxia-reoxygenation, significantly increased JNK 1 /SAPK 1 activation in cultured hepatocytes. Either in warm or cold conditions, OFR scavengers (N-Acetylcystein, Di-Phenyleneiodonium, Deferoxamine) decreased this stimulation. Warm ischemia-reperfusion also led to JNK activation. Hypoxia and especially hypoxia-reoxygenation induced programmed cell death in vivo and in vitro. This last phenomenon was inhibited when hepatocytes were treated with SB 202190, which was described as a potent inhibitor of p38 and JNK activities. Altogether, these results confirmed that JNK 1 /SAPK 1 was activated during the hypoxia-reoxygenation process, and that this activity participated in the onset of the apoptosis program. (HEPATOLOGY 2000;32:1029-1036.)

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“…These approaches often yield partial effects due to the redundancy of the various signaling molecules, and therefore may either incompletely suppress JNK activation or interfere with other pathways that influence survival. Nonetheless, such strategies have supported a role for JNK in mediating apoptosis in many models of oxidative stress (Zanke et al, 1996;Turner et al, 1998;Wang et al, 1998;Yin et al, 2000). Another approach that has provided support for the role of JNK in mediating apoptosis by oxidative stress is the use of antisense oligonucleotides possessing high specificity for different JNK isoforms (Garay et al, 2000;Hreniuk et al, 2001).…”

Section: Sapk Pathwaysmentioning

confidence: 99%

Cellular response to oxidative stress: Signaling for suicide and survival*

Martindale

Holbrook

2002

Journal Cellular Physiology

2,057

1,566

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Reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The importance of oxidative damage to the pathogenesis of many diseases as well as to degenerative processes of aging has becoming increasingly apparent over the past few years. Cells contain a number of antioxidant defenses to minimize fluctuations in ROS, but ROS generation often exceeds the cell's antioxidant capacity, resulting in a condition termed oxidative stress. Host survival depends upon the ability of cells and tissues to adapt to or resist the stress, and repair or remove damaged molecules or cells. Numerous stress response mechanisms have evolved for these purposes, and they are rapidly activated in response to oxidative insults. Some of the pathways are preferentially linked to enhanced survival, while others are more frequently associated with cell death. Still others have been implicated in both extremes depending on the particular circumstances. In this review, we discuss the various signaling pathways known to be activated in response to oxidative stress in mammalian cells, the mechanisms leading to their activation, and their roles in influencing cell survival. These pathways constitute important avenues for therapeutic interventions aimed at limiting oxidative damage or attenuating its sequelae. Published 2002 Wiley‐Liss, Inc.

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Oxidative Stress Induces DNA Fragmentation and Caspase Activation Via the c-Jun NH2-terminal Kinase Pathway in H9c2 Cardiac Muscle Cells

Cited by 180 publications

References 0 publications

The water extract of Omija protects H9c2 cardiomyoblast cells from hydrogen peroxide through prevention of mitochondrial dysfunction and activation of caspases pathway

The water extract of Omija protects H9c2 cardiomyoblast cells from hydrogen peroxide through prevention of mitochondrial dysfunction and activation of caspases pathway

Protein Kinase Activation by Warm And Cold Hypoxia- Reoxygenation in Primary-Cultured Rat Hepatocytes–JNK1/SAPK1 Involvement in Apoptosis

Cellular response to oxidative stress: Signaling for suicide and survival*

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