Sequential activation of activator protein-1-related transcription factors and JNK protein kinases may contribute to apoptotic death induced by transient hypoxia in developing brain neurons

Chihab, Rifki; Ferry, Céline; Koziel, Violette; Monin, Philippe; Daval, Jean‐Luc

doi:10.1016/s0169-328x(98)00266-6

Cited by 62 publications

(32 citation statements)

References 57 publications

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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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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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“…Interestingly, c-Jun is also activated as part of the stress response induced by UV radiation, peroxide, heat shock, and hypoxia (Bukh et al, 1990;Chihab et al, 1998;Devary et al, 1991;Diamond et al, 1999;Gilby et al, 1997;Rupec and Baeuerle, 1995). Although the mechanisms involved in Jun activation by these stress signals are complex, and involve both transcriptional as well as post-translational events, our results demonstrate a mechanism by which c-Jun translation can be eciently maintained so that it can regulate gene activity even under these adverse conditions.…”

Section: Discussionmentioning

confidence: 99%

The chicken c-Jun 5′ untranslated region directs translation by internal initiation

et al. 2000

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“…Hypoxia exposure increased c-Jun, Jun B, Jun D, c-Fos, and Fos-related protein expression. JNK-1 and JNK-3 both increased transiently 48 h after reoxygenation, when apoptosis occurred (22).…”

Section: Stress Kinases Jnk and Ap-1mentioning

confidence: 95%

Reactive species mechanisms of cellular hypoxia-reoxygenation injury

Jackson

2002

American Journal of Physiology-Cell Physiology

942

673

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Li, Chuanyu, and Robert M. Jackson. Reactive species mechanisms of cellular hypoxia-reoxygenation injury. Am J Physiol Cell Physiol 282: C227-C241, 2002; 10.1152/ajpcell.00112.2001.-Exacerbation of hypoxic injury after restoration of oxygenation (reoxygenation) is an important mechanism of cellular injury in transplantation and in myocardial, hepatic, intestinal, cerebral, renal, and other ischemic syndromes. Cellular hypoxia and reoxygenation are two essential elements of ischemia-reperfusion injury. Activated neutrophils contribute to vascular reperfusion injury, yet posthypoxic cellular injury occurs in the absence of inflammatory cells through mechanisms involving reactive oxygen (ROS) or nitrogen species (RNS). Xanthine oxidase (XO) produces ROS in some reoxygenated cells, but other intracellular sources of ROS are abundant, and XO is not required for reoxygenation injury. Hypoxic or reoxygenated mitochondria may produce excess superoxide (O 2 Ϫ ) and release H2O2, a diffusible long-lived oxidant that can activate signaling pathways or react vicinally with proteins and lipid membranes. This review focuses on the specific roles of ROS and RNS in the cellular response to hypoxia and subsequent cytolytic injury during reoxygenation.anoxia; ischemia; reperfusion BACKGROUND

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Sequential activation of activator protein-1-related transcription factors and JNK protein kinases may contribute to apoptotic death induced by transient hypoxia in developing brain neurons

Cited by 62 publications

References 57 publications

Protein Kinase Activation by Warm and Cold Hypoxia–Reoxygenation in Primary–Cultured Rat Hepatocytes-Jnk1/Sapk1 Involvement in Apoptosis

Protein Kinase Activation by Warm and Cold Hypoxia–Reoxygenation in Primary–Cultured Rat Hepatocytes-Jnk1/Sapk1 Involvement in Apoptosis

The chicken c-Jun 5′ untranslated region directs translation by internal initiation

Reactive species mechanisms of cellular hypoxia-reoxygenation injury

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