A Role for Mitogen- and Stress-Activated Kinase 1 in L-DOPA-Induced Dyskinesia and ∆FosB Expression.
Identifieur interne : 000179 ( PubMed/Corpus ); précédent : 000178; suivant : 000180A Role for Mitogen- and Stress-Activated Kinase 1 in L-DOPA-Induced Dyskinesia and ∆FosB Expression.
Auteurs : Michael Feyder ; Erik Södersten ; Emanuela Santini ; Vincent Vialou ; Quincey Laplant ; Emily L. Watts ; Giada Spigolon ; Klaus Hansen ; Jocelyne Caboche ; Eric J. Nestler ; Gilberto FisoneSource :
- Biological psychiatry [ 1873-2402 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Dyskinesia, Drug-Induced (metabolism), Extracellular Signal-Regulated MAP Kinases (drug effects), Histones (metabolism), Levodopa (adverse effects), Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Neostriatum (drug effects), Neurons (drug effects), Oxidopamine (administration & dosage), Parkinson Disease (complications), Phosphorylation, Proto-Oncogene Proteins c-fos (metabolism), Ribosomal Protein S6 Kinases, 90-kDa (metabolism).
- MESH :
- chemical , administration & dosage : Oxidopamine.
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , drug effects : Extracellular Signal-Regulated MAP Kinases.
- complications : Parkinson Disease.
- drug effects : Neostriatum, Neurons.
- metabolism : Dyskinesia, Drug-Induced, Histones, Proto-Oncogene Proteins c-fos, Ribosomal Protein S6 Kinases, 90-kDa.
- Animals, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Phosphorylation.
Abstract
Abnormal regulation of extracellular signal-regulated kinases 1 and 2 has been implicated in 3,4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication affecting Parkinson's disease patients subjected to standard pharmacotherapy. We examined the involvement of mitogen- and stress-activated kinase 1 (MSK1), a downstream target of extracellular signal-regulated kinases 1 and 2, and an important regulator of transcription in LID.
DOI: 10.1016/j.biopsych.2014.07.019
PubMed: 25193242
Links to Exploration step
pubmed:25193242Le document en format XML
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<term>Dyskinesia, Drug-Induced (metabolism)</term>
<term>Extracellular Signal-Regulated MAP Kinases (drug effects)</term>
<term>Histones (metabolism)</term>
<term>Levodopa (adverse effects)</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Neostriatum (drug effects)</term>
<term>Neurons (drug effects)</term>
<term>Oxidopamine (administration & dosage)</term>
<term>Parkinson Disease (complications)</term>
<term>Phosphorylation</term>
<term>Proto-Oncogene Proteins c-fos (metabolism)</term>
<term>Ribosomal Protein S6 Kinases, 90-kDa (metabolism)</term>
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<term>Proto-Oncogene Proteins c-fos</term>
<term>Ribosomal Protein S6 Kinases, 90-kDa</term>
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<term>Male</term>
<term>Mice</term>
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<front><div type="abstract" xml:lang="en">Abnormal regulation of extracellular signal-regulated kinases 1 and 2 has been implicated in 3,4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication affecting Parkinson's disease patients subjected to standard pharmacotherapy. We examined the involvement of mitogen- and stress-activated kinase 1 (MSK1), a downstream target of extracellular signal-regulated kinases 1 and 2, and an important regulator of transcription in LID.</div>
</front>
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<Month>02</Month>
<Day>05</Day>
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<DateCompleted><Year>2016</Year>
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<Day>17</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>12</Month>
<Day>30</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-2402</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>79</Volume>
<Issue>5</Issue>
<PubDate><Year>2016</Year>
<Month>Mar</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Biological psychiatry</Title>
<ISOAbbreviation>Biol. Psychiatry</ISOAbbreviation>
</Journal>
<ArticleTitle>A Role for Mitogen- and Stress-Activated Kinase 1 in L-DOPA-Induced Dyskinesia and ∆FosB Expression.</ArticleTitle>
<Pagination><MedlinePgn>362-71</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biopsych.2014.07.019</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0006-3223(14)00552-6</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Abnormal regulation of extracellular signal-regulated kinases 1 and 2 has been implicated in 3,4-dihydroxy-l-phenylalanine (L-DOPA)-induced dyskinesia (LID), a motor complication affecting Parkinson's disease patients subjected to standard pharmacotherapy. We examined the involvement of mitogen- and stress-activated kinase 1 (MSK1), a downstream target of extracellular signal-regulated kinases 1 and 2, and an important regulator of transcription in LID.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">6-Hydroxydopamine was used to produce a model of Parkinson's disease in MSK1 knockout mice and in ∆FosB- or ∆cJun-overexpressing transgenic mice, which were assessed for LID following long-term L-DOPA administration. Biochemical processes were evaluated by Western blotting or immunofluorescence. Histone H3 phosphorylation was analyzed by chromatin immunoprecipitation followed by promotor-specific quantitative polymerase chain reaction.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Genetic inactivation of MSK1 attenuated LID and reduced the phosphorylation of histone H3 at Ser10 in the striatum. Chromatin immunoprecipitation analysis showed that this reduction occurred at the level of the fosB gene promoter. In line with this observation, the accumulation of ∆FosB produced by chronic L-DOPA was reduced in MSK1 knockout. Moreover, inducible overexpression of ∆FosB in striatonigral medium spiny neurons exacerbated dyskinetic behavior, whereas overexpression of ∆cJun, which reduces ∆FosB-dependent transcriptional activation, counteracted LID.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Results indicate that abnormal regulation of MSK1 contributes to the development of LID and to the concomitant increase in striatal ∆FosB, which may occur via increased histone H3 phosphorylation at the fosB promoter. Results also show that accumulation of ∆FosB in striatonigral neurons is causally related to the development of dyskinesia.</AbstractText>
<CopyrightInformation>Copyright © 2016 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Feyder</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Södersten</LastName>
<ForeName>Erik</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden; Biotech Research and Innovation Centre and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Santini</LastName>
<ForeName>Emanuela</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
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<ForeName>Vincent</ForeName>
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<AffiliationInfo><Affiliation>Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York; Institut National de la Santé et de la Recherche Médicale, Le Centre national de la recherche scientifique Unités Mixtes de Recherche 7224, Université Pierre et Marie Curie, Paris, France.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
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<AffiliationInfo><Affiliation>Biotech Research and Innovation Centre and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark.</Affiliation>
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<ForeName>Jocelyne</ForeName>
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<AffiliationInfo><Affiliation>Institut National de la Santé et de la Recherche Médicale, Le Centre national de la recherche scientifique Unités Mixtes de Recherche 7224, Université Pierre et Marie Curie, Paris, France.</Affiliation>
</AffiliationInfo>
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<ForeName>Eric J</ForeName>
<Initials>EJ</Initials>
<AffiliationInfo><Affiliation>Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fisone</LastName>
<ForeName>Gilberto</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. Electronic address: gilberto.fisone@ki.se.</Affiliation>
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