MersV1, France, Analysis, bibRecord, 000246

6-hydroxydopamine-induced nuclear factor-kappaB activation in PC12 cells

Identifieur interne : 000246 ( France/Analysis ); précédent : 000245; suivant : 000247

6-hydroxydopamine-induced nuclear factor-kappaB activation in PC12 cells

Auteurs : David Blum [Belgique] ; Sakina Torch [France] ; Marie-France Nissou [France] ; Jean-Marc Verna [France]

Source :

Biochemical Pharmacology [ 0006-2952 ] ; 2001.

RBID : ISTEX:19A9544198C7423300F88E6C63BD319AE35E21FF

English descriptors

KwdEn :
- 6-Hydroxydopamine, Bcl-2, NF-kappaB, PC12 cells, Parkinson’s disease.
Teeft :
- Acad, Activation, Antibody santa cruz, Apoptosis, Assay, Biochem pharmacol, Biochemical pharmacology, Biol, Biol chem, Blum, Catecholaminergic, Cell cultures, Cell death, Cell death pathway, Cell line, Cell survival, Cell viability, Clear supershift, Consensus sequence, Constitutive activity, Crucial transcription factor, Culture medium, Cytoplasmic levels, Ectopic expression, Electrophoretic mobility shift assay, Elsevier science, Emsa, Emsa analysis, Equal amounts, Exact function, Further studies, Hippocampal neurons, Hydrogen peroxide, Immunoblot analysis, Independent experiments, Luciferase, Luciferase activity, Manganese superoxyde dismutase, Natl, Neuron, Neuronal, Neuronal cell death, Neuronal cell function, Neuronal cells, Neurosci, Neurosci lett, Neurotoxin, Nuclear content, Nuclear extracts, Nuclear factor kappab, Nuclear translocation, Oxidative, Oxidative stress, Parthenolide, Pathway, Peroxynitrite production, Pharmacology, Plasmid, Positive regulation, Present study, Proc, Proc natl acad, Protective effect, Protective effects, Protective mechanism, Protein tyrosine nitration, Quadruplicate determinations, Reactive oxygen intermediates, Recent studies, Representative experiment, Room temperature, Santa cruz, Sesquiterpene lactones, Several studies, Similar results, Target genes, Toxicity, Transcription, Transcription factor, Transcription factor activation, Transcription factors, Triplicate determinations, Tumor necrosis factor, Untreated, Untreated cells, Untreated control, Viability.

Abstract

Abstract: The involvement of nuclear Factor-kappaB (NF-κB) transcription factor in PC12 cell death triggered by the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) was investigated. Results show that oxidative stress generated by 6-OHDA activates NF-κB. When the NF-κB activation was inhibited by parthenolide, PC12 cell death induced by 6-OHDA was significantly increased, thus suggesting an involvement of this transcription factor in a protective mechanism against 6-OHDA toxicity. To further assess this hypothesis, we studied the involvement of NF-κB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1. Although Bcl-2 and Bfl-1 expression normally protects PC12 cells from 6-OHDA, parthenolide strongly decreased the beneficial effects afforded by transgene expression. These results suggest: (1) that the transcription factor NF-κB is likely associated with the protection of catecholaminergic PC12 cells and (2) that the protective effects afforded by bcl-2 and bfl-1 expression may be dependent on NF-κ activation.

Url:

https://api.istex.fr/ark:/67375/6H6-MG3361B1-9/fulltext.pdf

DOI: 10.1016/S0006-2952(01)00680-3

Affiliations:

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Le document en format XML

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<term>Parkinson’s disease</term>
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<term>Antibody santa cruz</term>
<term>Apoptosis</term>
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<term>Biochem pharmacol</term>
<term>Biochemical pharmacology</term>
<term>Biol</term>
<term>Biol chem</term>
<term>Blum</term>
<term>Catecholaminergic</term>
<term>Cell cultures</term>
<term>Cell death</term>
<term>Cell death pathway</term>
<term>Cell line</term>
<term>Cell survival</term>
<term>Cell viability</term>
<term>Clear supershift</term>
<term>Consensus sequence</term>
<term>Constitutive activity</term>
<term>Crucial transcription factor</term>
<term>Culture medium</term>
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<term>Ectopic expression</term>
<term>Electrophoretic mobility shift assay</term>
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<term>Emsa</term>
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<term>Equal amounts</term>
<term>Exact function</term>
<term>Further studies</term>
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<term>Hydrogen peroxide</term>
<term>Immunoblot analysis</term>
<term>Independent experiments</term>
<term>Luciferase</term>
<term>Luciferase activity</term>
<term>Manganese superoxyde dismutase</term>
<term>Natl</term>
<term>Neuron</term>
<term>Neuronal</term>
<term>Neuronal cell death</term>
<term>Neuronal cell function</term>
<term>Neuronal cells</term>
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<term>Neurosci lett</term>
<term>Neurotoxin</term>
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<term>Nuclear extracts</term>
<term>Nuclear factor kappab</term>
<term>Nuclear translocation</term>
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<term>Oxidative stress</term>
<term>Parthenolide</term>
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<term>Peroxynitrite production</term>
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<term>Plasmid</term>
<term>Positive regulation</term>
<term>Present study</term>
<term>Proc</term>
<term>Proc natl acad</term>
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<term>Protective effects</term>
<term>Protective mechanism</term>
<term>Protein tyrosine nitration</term>
<term>Quadruplicate determinations</term>
<term>Reactive oxygen intermediates</term>
<term>Recent studies</term>
<term>Representative experiment</term>
<term>Room temperature</term>
<term>Santa cruz</term>
<term>Sesquiterpene lactones</term>
<term>Several studies</term>
<term>Similar results</term>
<term>Target genes</term>
<term>Toxicity</term>
<term>Transcription</term>
<term>Transcription factor</term>
<term>Transcription factor activation</term>
<term>Transcription factors</term>
<term>Triplicate determinations</term>
<term>Tumor necrosis factor</term>
<term>Untreated</term>
<term>Untreated cells</term>
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<front><div type="abstract" xml:lang="en">Abstract: The involvement of nuclear Factor-kappaB (NF-κB) transcription factor in PC12 cell death triggered by the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) was investigated. Results show that oxidative stress generated by 6-OHDA activates NF-κB. When the NF-κB activation was inhibited by parthenolide, PC12 cell death induced by 6-OHDA was significantly increased, thus suggesting an involvement of this transcription factor in a protective mechanism against 6-OHDA toxicity. To further assess this hypothesis, we studied the involvement of NF-κB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1. Although Bcl-2 and Bfl-1 expression normally protects PC12 cells from 6-OHDA, parthenolide strongly decreased the beneficial effects afforded by transgene expression. These results suggest: (1) that the transcription factor NF-κB is likely associated with the protection of catecholaminergic PC12 cells and (2) that the protective effects afforded by bcl-2 and bfl-1 expression may be dependent on NF-κ activation.</div>
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6-hydroxydopamine-induced nuclear factor-kappaB activation in PC12 cells

6-hydroxydopamine-induced nuclear factor-kappaB activation in PC12 cells

Source :

English descriptors

Abstract

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