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
Links to Exploration step
pubmed:9207126Le document en format XML
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Ricard</name></author><author><name sortKey="Michel, P P" sort="Michel, P P" uniqKey="Michel P" first="P P" last="Michel">P P Michel</name></author><author><name sortKey="Muriel, M P" sort="Muriel, M P" uniqKey="Muriel M" first="M P" last="Muriel">M P Muriel</name></author><author><name sortKey="Ruberg, M" sort="Ruberg, M" uniqKey="Ruberg M" first="M" last="Ruberg">M. Ruberg</name></author><author><name sortKey="Faucheux, B A" sort="Faucheux, B A" uniqKey="Faucheux B" first="B A" last="Faucheux">B A Faucheux</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9207126</idno><idno type="pmid">9207126</idno><idno type="wicri:Area/PubMed/Corpus">001519</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001519</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Nuclear translocation of NF-kappaB is increased in dopaminergic neurons of patients with parkinson disease.</title><author><name sortKey="Hunot, S" sort="Hunot, S" uniqKey="Hunot S" first="S" last="Hunot">S. Hunot</name><affiliation><nlm:affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 289, Mécanismes et Conséquences de la Mort Neuronale, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, F-75013 Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Brugg, B" sort="Brugg, B" uniqKey="Brugg B" first="B" last="Brugg">B. Brugg</name></author><author><name sortKey="Ricard, D" sort="Ricard, D" uniqKey="Ricard D" first="D" last="Ricard">D. Ricard</name></author><author><name sortKey="Michel, P P" sort="Michel, P P" uniqKey="Michel P" first="P P" last="Michel">P P Michel</name></author><author><name sortKey="Muriel, M P" sort="Muriel, M P" uniqKey="Muriel M" first="M P" last="Muriel">M P Muriel</name></author><author><name sortKey="Ruberg, M" sort="Ruberg, M" uniqKey="Ruberg M" first="M" last="Ruberg">M. Ruberg</name></author><author><name sortKey="Faucheux, B A" sort="Faucheux, B A" uniqKey="Faucheux B" first="B A" last="Faucheux">B A Faucheux</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Biological Transport</term><term>Cell Nucleus (metabolism)</term><term>Cell Nucleus (ultrastructure)</term><term>Cells, Cultured</term><term>Dopamine</term><term>Humans</term><term>Microscopy, Electron</term><term>NF-kappa B (metabolism)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Rats</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NF-kappa B</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Nucleus</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Cell Nucleus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Biological Transport</term><term>Cells, Cultured</term><term>Humans</term><term>Microscopy, Electron</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9207126</PMID><DateCreated><Year>1997</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>1997</Year><Month>08</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0027-8424</ISSN><JournalIssue CitedMedium="Print"><Volume>94</Volume><Issue>14</Issue><PubDate><Year>1997</Year><Month>Jul</Month><Day>08</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>Nuclear translocation of NF-kappaB is increased in dopaminergic neurons of patients with parkinson disease.</ArticleTitle><Pagination><MedlinePgn>7531-6</MedlinePgn></Pagination><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></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hunot</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 289, Mécanismes et Conséquences de la Mort Neuronale, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, F-75013 Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brugg</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Ricard</LastName><ForeName>D</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Michel</LastName><ForeName>P P</ForeName><Initials>PP</Initials></Author><Author ValidYN="Y"><LastName>Muriel</LastName><ForeName>M P</ForeName><Initials>MP</Initials></Author><Author ValidYN="Y"><LastName>Ruberg</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Faucheux</LastName><ForeName>B A</ForeName><Initials>BA</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Nature. 1988 Jul 28;334(6180):345-8</RefSource><PMID Version="1">2899295</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1984 Sep;81(17):5613-7</RefSource><PMID Version="1">6591209</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 1989 Sep;53(3):692-7</RefSource><PMID Version="1">2760616</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Genes Dev. 1989 Nov;3(11):1689-98</RefSource><PMID Version="1">2691328</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 1991 Feb;56(2):446-51</RefSource><PMID Version="1">1988548</PMID></CommentsCorrections><CommentsCorrections 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MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008854" MajorTopicYN="N">Microscopy, Electron</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC23856</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>7</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>7</Month><Day>8</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>7</Month><Day>8</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9207126</ArticleId><ArticleId IdType="pmc">PMC23856</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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