6-hydroxydopamine-induced nuclear factor-kappab activation in PC12 cells
Identifieur interne : 000234 ( PascalFrancis/Curation ); précédent : 000233; suivant : 0002356-hydroxydopamine-induced nuclear factor-kappab activation in PC12 cells
Auteurs : David Blum [Belgique, France] ; Sakina Torch [France] ; Marie-France Nissou [France] ; Jean-Marc Verna [France]Source :
- Biochemical pharmacology [ 0006-2952 ] ; 2001.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
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-KB. When the NF-KB 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-KB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1 Although Bcl-2 and Bfl- I 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-KB 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-KB activation.
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Pascal:01-0372250Le document en format XML
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<term>Cell death</term>
<term>Dopamine</term>
<term>Established cell line</term>
<term>Gene expression</term>
<term>Human</term>
<term>Neuron</term>
<term>Neurotoxin</term>
<term>Oxidative stress</term>
<term>Oxidopamine</term>
<term>Parkinson disease</term>
<term>Sympathomimetic</term>
<term>Toxicity</term>
<term>Transcription factor NFκB</term>
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<term>Sympathomimétique</term>
<term>Neurotoxine</term>
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<term>Lignée cellulaire établie</term>
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<term>Parkinson maladie</term>
<term>Homme</term>
<term>Dopamine</term>
<term>Activation</term>
<term>Toxicité</term>
<term>Expression génique</term>
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<term>Neurone</term>
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<front><div type="abstract" xml:lang="en">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-KB. When the NF-KB 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-KB in the protective effect of two anti-apoptotic genes, bcl-2 and bfl-1 Although Bcl-2 and Bfl- I 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-KB 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-KB activation.</div>
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