Gene expression analyses identify Narp contribution in the development of L-DOPA-induced dyskinesia.
Identifieur interne : 000407 ( PubMed/Curation ); précédent : 000406; suivant : 000408Gene expression analyses identify Narp contribution in the development of L-DOPA-induced dyskinesia.
Auteurs : Fanny Charbonnier-Beaupel [France] ; Marion Malerbi [France] ; Cristina Alcacer [France] ; Khadija Tahiri [France] ; Wassila Carpentier [France] ; Chuansong Wang [États-Unis] ; Matthew During [États-Unis] ; Desheng Xu ; Paul F. Worley ; Jean-Antoine Girault [France] ; Denis Hervé [France] ; Jean-Christophe Corvol [France]Source :
- The Journal of neuroscience : the official journal of the Society for Neuroscience [ 1529-2401 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (toxicity), C-Reactive Protein (biosynthesis), C-Reactive Protein (genetics), Dyskinesia, Drug-Induced (genetics), Dyskinesia, Drug-Induced (metabolism), Dyskinesia, Drug-Induced (pathology), Female, Gene Expression Regulation, Levodopa (toxicity), Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Nerve Tissue Proteins (biosynthesis), Nerve Tissue Proteins (genetics).
- MESH :
- chemical , biosynthesis : C-Reactive Protein, Nerve Tissue Proteins.
- chemical , genetics : C-Reactive Protein, Nerve Tissue Proteins.
- chemical , toxicity : Antiparkinson Agents, Levodopa.
- genetics : Dyskinesia, Drug-Induced.
- metabolism : Dyskinesia, Drug-Induced.
- pathology : Dyskinesia, Drug-Induced.
- Animals, Female, Gene Expression Regulation, Male, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
In Parkinson's disease, long-term dopamine replacement therapy is complicated by the appearance of L-DOPA-induced dyskinesia (LID). One major hypothesis is that LID results from an aberrant transcriptional program in striatal neurons induced by L-DOPA and triggered by the activation of ERK. To identify these genes, we performed transcriptome analyses in the striatum in 6-hydroxydopamine-lesioned mice. A time course analysis (0-6 h after treatment with L-DOPA) identified an acute signature of 709 genes, among which genes involved in protein phosphatase activity were overrepresented, suggesting a negative feedback on ERK activation by l-DOPA. l-DOPA-dependent deregulation of 28 genes was blocked by pretreatment with SL327, an inhibitor of ERK activation, and 26 genes were found differentially expressed between highly and weakly dyskinetic animals after treatment with L-DOPA. The intersection list identified five genes: FosB, Th, Nptx2, Nedd4l, and Ccrn4l. Nptx2 encodes neuronal pentraxin II (or neuronal activity-regulated pentraxin, Narp), which is involved in the clustering of glutamate receptors. We confirmed increased Nptx2 expression after L-DOPA and its blockade by SL327 using quantitative RT-PCR in independent experiments. Using an escalating L-DOPA dose protocol, LID severity was decreased in Narp knock-out mice compared with their wild-type littermates or after overexpression of a dominant-negative form of Narp in the striatum. In conclusion, we have identified a molecular signature induced by L-DOPA in the dopamine-denervated striatum that is dependent on ERK and associated with LID. Here, we demonstrate the implication of one of these genes, Nptx2, in the development of LID.
DOI: 10.1523/JNEUROSCI.5231-13.2015
PubMed: 25568106
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Desheng Xu<affiliation><nlm:affiliation>Johns Hopkins University School of Medicine, Solomon H. Snyder Department of Neuroscience, Baltimore, Maryland 21205, and.</nlm:affiliation>
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<term>C-Reactive Protein (biosynthesis)</term>
<term>C-Reactive Protein (genetics)</term>
<term>Dyskinesia, Drug-Induced (genetics)</term>
<term>Dyskinesia, Drug-Induced (metabolism)</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dyskinesia, Drug-Induced</term>
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<front><div type="abstract" xml:lang="en">In Parkinson's disease, long-term dopamine replacement therapy is complicated by the appearance of L-DOPA-induced dyskinesia (LID). One major hypothesis is that LID results from an aberrant transcriptional program in striatal neurons induced by L-DOPA and triggered by the activation of ERK. To identify these genes, we performed transcriptome analyses in the striatum in 6-hydroxydopamine-lesioned mice. A time course analysis (0-6 h after treatment with L-DOPA) identified an acute signature of 709 genes, among which genes involved in protein phosphatase activity were overrepresented, suggesting a negative feedback on ERK activation by l-DOPA. l-DOPA-dependent deregulation of 28 genes was blocked by pretreatment with SL327, an inhibitor of ERK activation, and 26 genes were found differentially expressed between highly and weakly dyskinetic animals after treatment with L-DOPA. The intersection list identified five genes: FosB, Th, Nptx2, Nedd4l, and Ccrn4l. Nptx2 encodes neuronal pentraxin II (or neuronal activity-regulated pentraxin, Narp), which is involved in the clustering of glutamate receptors. We confirmed increased Nptx2 expression after L-DOPA and its blockade by SL327 using quantitative RT-PCR in independent experiments. Using an escalating L-DOPA dose protocol, LID severity was decreased in Narp knock-out mice compared with their wild-type littermates or after overexpression of a dominant-negative form of Narp in the striatum. In conclusion, we have identified a molecular signature induced by L-DOPA in the dopamine-denervated striatum that is dependent on ERK and associated with LID. Here, we demonstrate the implication of one of these genes, Nptx2, in the development of LID.</div>
</front>
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<ISOAbbreviation>J. Neurosci.</ISOAbbreviation>
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<ArticleTitle>Gene expression analyses identify Narp contribution in the development of L-DOPA-induced dyskinesia.</ArticleTitle>
<Pagination><MedlinePgn>96-111</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1523/JNEUROSCI.5231-13.2015</ELocationID>
<Abstract><AbstractText>In Parkinson's disease, long-term dopamine replacement therapy is complicated by the appearance of L-DOPA-induced dyskinesia (LID). One major hypothesis is that LID results from an aberrant transcriptional program in striatal neurons induced by L-DOPA and triggered by the activation of ERK. To identify these genes, we performed transcriptome analyses in the striatum in 6-hydroxydopamine-lesioned mice. A time course analysis (0-6 h after treatment with L-DOPA) identified an acute signature of 709 genes, among which genes involved in protein phosphatase activity were overrepresented, suggesting a negative feedback on ERK activation by l-DOPA. l-DOPA-dependent deregulation of 28 genes was blocked by pretreatment with SL327, an inhibitor of ERK activation, and 26 genes were found differentially expressed between highly and weakly dyskinetic animals after treatment with L-DOPA. The intersection list identified five genes: FosB, Th, Nptx2, Nedd4l, and Ccrn4l. Nptx2 encodes neuronal pentraxin II (or neuronal activity-regulated pentraxin, Narp), which is involved in the clustering of glutamate receptors. We confirmed increased Nptx2 expression after L-DOPA and its blockade by SL327 using quantitative RT-PCR in independent experiments. Using an escalating L-DOPA dose protocol, LID severity was decreased in Narp knock-out mice compared with their wild-type littermates or after overexpression of a dominant-negative form of Narp in the striatum. In conclusion, we have identified a molecular signature induced by L-DOPA in the dopamine-denervated striatum that is dependent on ERK and associated with LID. Here, we demonstrate the implication of one of these genes, Nptx2, in the development of LID.</AbstractText>
<CopyrightInformation>Copyright © 2015 the authors 0270-6474/15/350096-16$15.00/0.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Charbonnier-Beaupel</LastName>
<ForeName>Fanny</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Sorbonne Universités, UPMC Univ Paris 06, Paris, France, Inserm, UMR-S 1127, ICM, Pitié-Salpêtrière Hospital, 75013 Paris, France, CNRS, UMR 7225, 75013 Paris, France, Assistance Publique Hôpitaux de Paris, Department of Pharmacy, Pitié-Salpêtrière Hospital, 75013 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Malerbi</LastName>
<ForeName>Marion</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Sorbonne Universités, UPMC Univ Paris 06, Paris, France, Inserm, UMR-S 1127, ICM, Pitié-Salpêtrière Hospital, 75013 Paris, France, CNRS, UMR 7225, 75013 Paris, France, Inserm UMR-S 839, 75005 Paris, France, Institut du Fer à Moulin, 75005 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Alcacer</LastName>
<ForeName>Cristina</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Sorbonne Universités, UPMC Univ Paris 06, Paris, France, Inserm UMR-S 839, 75005 Paris, France, Institut du Fer à Moulin, 75005 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tahiri</LastName>
<ForeName>Khadija</ForeName>
<Initials>K</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-1039-8126</Identifier>
<AffiliationInfo><Affiliation>Sorbonne Universités, UPMC Univ Paris 06, Paris, France, Inserm, UMR-S 1127, ICM, Pitié-Salpêtrière Hospital, 75013 Paris, France, CNRS, UMR 7225, 75013 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Carpentier</LastName>
<ForeName>Wassila</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>UPMC Univ Paris 06, Post genomic platform P3S, 75013 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Chuansong</ForeName>
<Initials>C</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0003-4501-2518</Identifier>
<AffiliationInfo><Affiliation>Departments of Molecular Virology, Immunology and Medical Genetics, Neuroscience and Neurological Surgery, The Ohio State University, Columbus, Ohio 43210.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>During</LastName>
<ForeName>Matthew</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Departments of Molecular Virology, Immunology and Medical Genetics, Neuroscience and Neurological Surgery, The Ohio State University, Columbus, Ohio 43210.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Desheng</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Johns Hopkins University School of Medicine, Solomon H. Snyder Department of Neuroscience, Baltimore, Maryland 21205, and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Worley</LastName>
<ForeName>Paul F</ForeName>
<Initials>PF</Initials>
<AffiliationInfo><Affiliation>Johns Hopkins University School of Medicine, Solomon H. Snyder Department of Neuroscience, Baltimore, Maryland 21205, and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Girault</LastName>
<ForeName>Jean-Antoine</ForeName>
<Initials>JA</Initials>
<AffiliationInfo><Affiliation>Sorbonne Universités, UPMC Univ Paris 06, Paris, France, Inserm UMR-S 839, 75005 Paris, France, Institut du Fer à Moulin, 75005 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hervé</LastName>
<ForeName>Denis</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Sorbonne Universités, UPMC Univ Paris 06, Paris, France, Inserm UMR-S 839, 75005 Paris, France, Institut du Fer à Moulin, 75005 Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Corvol</LastName>
<ForeName>Jean-Christophe</ForeName>
<Initials>JC</Initials>
<AffiliationInfo><Affiliation>Sorbonne Universités, UPMC Univ Paris 06, Paris, France, Inserm, UMR-S 1127, ICM, Pitié-Salpêtrière Hospital, 75013 Paris, France, CNRS, UMR 7225, 75013 Paris, France, Assistance Publique Hôpitaux de Paris, Inserm, Clinical Investigation Center, CIC-1422, Pitié-Salpêtrière Hospital, 75013 Paris, France jean-christophe.corvol@psl.aphp.fr.</Affiliation>
</AffiliationInfo>
</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>J Neurosci</MedlineTA>
<NlmUniqueID>8102140</NlmUniqueID>
<ISSNLinking>0270-6474</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C092775">neuronal pentraxin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>46627O600J</RegistryNumber>
<NameOfSubstance UI="D007980">Levodopa</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>9007-41-4</RegistryNumber>
<NameOfSubstance UI="D002097">C-Reactive Protein</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName>
<QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002097" MajorTopicYN="N">C-Reactive Protein</DescriptorName>
<QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName>
<QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009419" MajorTopicYN="N">Nerve Tissue Proteins</DescriptorName>
<QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Narp</Keyword>
<Keyword MajorTopicYN="N">Parkinson's disease</Keyword>
<Keyword MajorTopicYN="N">l-DOPA-induced dyskinesia</Keyword>
<Keyword MajorTopicYN="N">transcriptome</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2015</Year>
<Month>1</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2015</Year>
<Month>1</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2015</Year>
<Month>3</Month>
<Day>21</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25568106</ArticleId>
<ArticleId IdType="pii">35/1/96</ArticleId>
<ArticleId IdType="doi">10.1523/JNEUROSCI.5231-13.2015</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
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