Activity and expression of JNK1, p38 and ERK kinases, c-Jun N-terminal phosphorylation, and c-jun promoter binding in the adult rat brain following kainate-induced seizures

Mielke, Kirsten; Brecht, Stephan; Dorst, Annika; Herdegen, Thomas

doi:10.1016/s0306-4522(98)00667-8

Cited by 117 publications

(67 citation statements)

References 62 publications

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“…injection. Several studies reported that the p-ERK was increased by systemic administration of KA in the rat hippocampus (Mielke et al, 1999;Jeon et al, 2000). Recent studies showed that seizures induced the sprouting of mossy fibers in the rat hippocampus CA3 region (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…KA, administered i.c.v., induced the lesion of CA3 pyramidal neurons in mice (Ferraguti et al, 2001;Lee et al, 2002;Lee et al, 2003). The phosphorylated extracellular signal-regulated kinase (p-ERK) is increased by systemic administration of KA in the rat hippocampus (Mielke et al, 1999;Jeon et al, 2000). Seizures induce the sprouting of mossy fibers in the CA3 region of rat hippocampus (Ben-Ari and Cossart, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Role of γ-aminobutyric acid B (GABAB) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus

Lee

Seo²,

Choi³

et al. 2005

Exp Mol Med

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of γ-aminobutyric acid B (GABAB) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus

Lee

Seo²,

Choi³

et al. 2005

Exp Mol Med

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“…The MKKs are activated by a group of upstream kinases known as the MAP kinase kinase kinases (MKKKs). This cascade is triggered under a variety of cellular stresses and has also been observed in the hippocampus after seizures elicited by diverse means Herdegen et al, 1998;Brecht et al, 1999;Mielke et al, 1999;Jeon et al, 2000). Numerous studies have demonstrated the importance of JNK activation in promoting excitotoxic neuronal death in the CNS (Mattson and Bazan, 2006).…”

Section: Introductionmentioning

confidence: 93%

c-Jun N-Terminal Kinase Activation Responses Induced by Hippocampal Kindling Are Mediated by Reactive Astrocytes

Cole-Edwards¹,

Musto²,

Bazán³

2006

J. Neurosci.

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Hippocampal kindling, a model of mesial temporal lobe epilepsy, is developed through repetitive stimulation of the hippocampus and leads to increased after-discharges as measured by EEG and an enduring seizure-prone state. Synthesis of new proteins is thought to form the basis for sustained seizure-induced physiological and/or pathological changes in synaptic reorganization and apoptotic/necrotic neuronal death. Here we examined the effect of kindling on stimulus-induced c-Jun N-terminal kinase (JNK) and p38 phosphorylation, events postulated to lie upstream of seizure-induced changes in gene transcription. We found that stimulus-induced phosphorylation of JNK, but not of p38, is significantly enhanced in kindled animals compared with their naive counterparts in the CA1 subregion of the hippocampus. Immunofluorescent staining confirmed this region-specific pattern of JNK activation and revealed that reactive astrocytes mediate this effect. Astrocyte proliferation and hypertrophy, as well as upregulation of vimentin protein levels, common markers of astrogliosis, were present after 4 d of kindling. Moreover, this reactive astrogliosis was associated with neuronal death as visualized with Fluoro-jade B and anti-active caspase-3 staining. Stimulus-induced phosphorylation of the JNK substrate paxillin was enhanced in kindled animals, but not that of c-Jun. Moreover, a pan-antibody against MAPK/CDK (mitogen-activated protein kinases/cyclindependent kinase) substrates indicated the presence of phosphorylated proteins in cytosolic, membrane, and nuclear fractions. The consequence of these phosphorylation events is not completely understood, but these findings suggest a selective astrocytic signaling response to aberrant synaptic activity, signaling that may modulate kindling progression and/or neuronal death.

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“…However, the inhibition of ERK1/2 activation has been shown to protect a mouse neuronal cell line and rat primary cortical neurons form oxidative stress-induced neurotoxicity [1] demonstrating a possible involvement in cell death. The JNK signaling cascade has been reported to be activated by a wide range of different oxidants/reductants including hydrogen peroxide [135,218], lipid peroxidation products [6,191], different types of radiation [63], modulators of intracellular glutathione status [145], peroxynitrite [71], glutamate [180], dithiothreitol, and nitric oxide [152]. Although the links between redox status and MAPK signaling have been known for some time, data demonstrating the molecular basis of such links and identifying the sensors in this redox response are few.…”

Section: Mapk Signaling Under Oxidative Stressmentioning

confidence: 99%

“…The vectorial release of mitochondrial O 2 − (more correctly, H 2 O 2 ) to the cytosol may, in turn, be important in cell signaling [143], e.g. activation of MAPK such as JNK [135,218]. Indeed, a wealth of data on apoptosis is accumulating and emphasizing the potential role of the MAPK signaling cascade and mitochondrial function.…”

Section: Apoptosis Mitochondrial Function and Mapk Signal Transductionmentioning

confidence: 99%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

308

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

show abstract

Activity and expression of JNK1, p38 and ERK kinases, c-Jun N-terminal phosphorylation, and c-jun promoter binding in the adult rat brain following kainate-induced seizures

Cited by 117 publications

References 62 publications

Role of γ-aminobutyric acid B (GABAB) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus

Role of γ-aminobutyric acid B (GABAB) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus

c-Jun N-Terminal Kinase Activation Responses Induced by Hippocampal Kindling Are Mediated by Reactive Astrocytes

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

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