Nuclear translocation of NF-kappaB is increased in dopaminergic neurons of patients with parkinson disease.
Identifieur interne : 001519 ( PubMed/Corpus ); précédent : 001518; suivant : 001520Nuclear translocation of NF-kappaB is increased in dopaminergic neurons of patients with parkinson disease.
Auteurs : S. Hunot ; B. Brugg ; D. Ricard ; P P Michel ; M P Muriel ; M. Ruberg ; B A Faucheux ; Y. Agid ; E C HirschSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 1997.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Animals, Biological Transport, Cell Nucleus (metabolism), Cell Nucleus (ultrastructure), Cells, Cultured, Dopamine, Humans, Microscopy, Electron, NF-kappa B (metabolism), Neurons (metabolism), Neurons (pathology), Parkinson Disease (metabolism), Parkinson Disease (pathology), Rats.
- MESH :
- chemical , metabolism : NF-kappa B.
- chemical : Dopamine.
- metabolism : Cell Nucleus, Neurons, Parkinson Disease.
- pathology : Neurons, Parkinson Disease.
- ultrastructure : Cell Nucleus.
- Aged, Aged, 80 and over, Animals, Biological Transport, Cells, Cultured, Humans, Microscopy, Electron, Rats.
Abstract
Evidence from postmortem studies suggest an involvement of oxidative stress in the degeneration of dopaminergic neurons in Parkinson disease (PD) that have recently been shown to die by apoptosis, but the relationship between oxidative stress and apoptosis has not yet been elucidated. Activation of the transcription factor NF-kappaB is associated with oxidative stress-induced apoptosis in several nonneuronal in vitro models. To investigate whether it may play a role in PD, we looked for the translocation of NF-kappaB from the cytoplasm to the nucleus, evidence of its activation, in melanized neurons in the mesencephalon of postmortem human brain from five patients with idiopathic PD and seven matched control subjects. In PD patients, the proportion of dopaminergic neurons with immunoreactive NF-kappaB in their nuclei was more than 70-fold that in control subjects. A possible relationship between the nuclear localization of NF-kappaB in mesencephalic neurons of PD patients and oxidative stress in such neurons has been shown in vitro with primary cultures of rat mesencephalon, where translocation of NF-kappaB is preceded by a transient production of free radicals during apoptosis induced by activation of the sphingomyelin-dependent signaling pathway with C2-ceramide. The data suggest that this oxidant-mediated apoptogenic transduction pathway may play a role in the mechanism of neuronal death in PD.
PubMed: 9207126
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pubmed:9207126Le document en format XML
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<front><div type="abstract" xml:lang="en">Evidence from postmortem studies suggest an involvement of oxidative stress in the degeneration of dopaminergic neurons in Parkinson disease (PD) that have recently been shown to die by apoptosis, but the relationship between oxidative stress and apoptosis has not yet been elucidated. Activation of the transcription factor NF-kappaB is associated with oxidative stress-induced apoptosis in several nonneuronal in vitro models. To investigate whether it may play a role in PD, we looked for the translocation of NF-kappaB from the cytoplasm to the nucleus, evidence of its activation, in melanized neurons in the mesencephalon of postmortem human brain from five patients with idiopathic PD and seven matched control subjects. In PD patients, the proportion of dopaminergic neurons with immunoreactive NF-kappaB in their nuclei was more than 70-fold that in control subjects. A possible relationship between the nuclear localization of NF-kappaB in mesencephalic neurons of PD patients and oxidative stress in such neurons has been shown in vitro with primary cultures of rat mesencephalon, where translocation of NF-kappaB is preceded by a transient production of free radicals during apoptosis induced by activation of the sphingomyelin-dependent signaling pathway with C2-ceramide. The data suggest that this oxidant-mediated apoptogenic transduction pathway may play a role in the mechanism of neuronal death in PD.</div>
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<Abstract><AbstractText>Evidence from postmortem studies suggest an involvement of oxidative stress in the degeneration of dopaminergic neurons in Parkinson disease (PD) that have recently been shown to die by apoptosis, but the relationship between oxidative stress and apoptosis has not yet been elucidated. Activation of the transcription factor NF-kappaB is associated with oxidative stress-induced apoptosis in several nonneuronal in vitro models. To investigate whether it may play a role in PD, we looked for the translocation of NF-kappaB from the cytoplasm to the nucleus, evidence of its activation, in melanized neurons in the mesencephalon of postmortem human brain from five patients with idiopathic PD and seven matched control subjects. In PD patients, the proportion of dopaminergic neurons with immunoreactive NF-kappaB in their nuclei was more than 70-fold that in control subjects. A possible relationship between the nuclear localization of NF-kappaB in mesencephalic neurons of PD patients and oxidative stress in such neurons has been shown in vitro with primary cultures of rat mesencephalon, where translocation of NF-kappaB is preceded by a transient production of free radicals during apoptosis induced by activation of the sphingomyelin-dependent signaling pathway with C2-ceramide. The data suggest that this oxidant-mediated apoptogenic transduction pathway may play a role in the mechanism of neuronal death in PD.</AbstractText>
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