ParkinsonFranceV1, Hal, Checkpoint, bibRecord, 000108

Striatal NELF-mediated RNA polymerase II stalling controls l-dopa induced dyskinesia.

Identifieur interne : 000108 ( Hal/Checkpoint ); précédent : 000107; suivant : 000109

Striatal NELF-mediated RNA polymerase II stalling controls l-dopa induced dyskinesia.

Auteurs : Matthieu F. Bastide [France] ; Simone Bido [France] ; Nathalie Duteil [France] ; Erwan Bézard [France]

Source :

Neurobiology of Disease [ 0969-9961 ] ; 2015-12-31.

RBID : Hal:hal-01286252

Abstract

Long-term l-3,4-dihydroxyphenylalanine (l-Dopa) treatment in Parkinson's disease leads to involuntary movements called dyskinesia, notably through an overexpression of immediate-early genes (IEG). Their rapid transcription involves the stalling of RNA polymerase II on IEG promoters, a mechanism that critically depends on the presence of the negative elongation factor (NELF) protein complex. We here down-regulated the key NELF-E subunit using lentiviral vector delivery of a short hairpin RNA in the striatum of 6-hydroxydopamine lesioned rats. Such NELF-E reduced expression significantly attenuated the development of abnormal involuntary movements in response to chronic l-Dopa treatment. Effectiveness of silencing was demonstrated by the significant decrease in striatal ∆FosB, ARC and Zif268 IEG expression. Repression of NELF-mediating RNA polymerase II stalling thus achieves both antidyskinetic and potentiation of antiparkinsonian l-Dopa effect, highlighting the role of transcriptional events in dyskinesia establishment, acute dyskinetic manifestation and in the therapeutic response to l-Dopa.

Url:

https://hal.archives-ouvertes.fr/hal-01286252

DOI: 10.1016/j.nbd

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Long-term l-3,4-dihydroxyphenylalanine (l-Dopa) treatment in Parkinson's disease leads to involuntary movements called dyskinesia, notably through an overexpression of immediate-early genes (IEG). Their rapid transcription involves the stalling of RNA polymerase II on IEG promoters, a mechanism that critically depends on the presence of the negative elongation factor (NELF) protein complex. We here down-regulated the key NELF-E subunit using lentiviral vector delivery of a short hairpin RNA in the striatum of 6-hydroxydopamine lesioned rats. Such NELF-E reduced expression significantly attenuated the development of abnormal involuntary movements in response to chronic l-Dopa treatment. Effectiveness of silencing was demonstrated by the significant decrease in striatal ∆FosB, ARC and Zif268 IEG expression. Repression of NELF-mediating RNA polymerase II stalling thus achieves both antidyskinetic and potentiation of antiparkinsonian l-Dopa effect, highlighting the role of transcriptional events in dyskinesia establishment, acute dyskinetic manifestation and in the therapeutic response to l-Dopa.</div>
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                <email type="md5">eb4bde61f74652335183b0bd05630b2c</email>
                <email type="domain">u-bordeaux.fr</email>
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            <idno type="halId">hal-01286252</idno>
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            <idno type="halBibtex">bastide:hal-01286252</idno>
            <idno type="halRefHtml">Neurobiology of Disease, Elsevier, 2015, 85, pp.93-8. <10.1016/j.nbd></idno>
            <idno type="halRef">Neurobiology of Disease, Elsevier, 2015, 85, pp.93-8. <10.1016/j.nbd></idno>
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            <note type="popular" n="0">No</note>
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          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="it">Striatal NELF-mediated RNA polymerase II stalling controls l-dopa induced dyskinesia.</title>
                <author role="aut">                  <persName>                    <forename type="first">Matthieu F</forename>
                    <surname>Bastide</surname>
                  </persName>
                  <idno type="halauthorid">1307903</idno>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Simone</forename>
                    <surname>Bido</surname>
                  </persName>
                  <idno type="halauthorid">1169071</idno>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Nathalie</forename>
                    <surname>Duteil</surname>
                  </persName>
                  <idno type="halauthorid">1307904</idno>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Erwan</forename>
                    <surname>Bézard</surname>
                  </persName>
                  <idno type="halauthorid">1063976</idno>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">13277</idno>
                <idno type="issn">0969-9961</idno>
                <idno type="eissn">1095-953X</idno>
                <title level="j">Neurobiology of Disease</title>
                <imprint>                  <publisher>Elsevier</publisher>
                  <biblScope unit="volume">85</biblScope>
                  <biblScope unit="pp">93-8</biblScope>
                  <date type="datePub">2015-12-31</date>
                </imprint>
              </monogr>
              <idno type="pubmed">26480869</idno>
              <idno type="doi">10.1016/j.nbd</idno>
            </biblStruct>
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            <textClass>              <classCode scheme="halDomain" n="sdv">Life Sciences [q-bio]</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">Long-term l-3,4-dihydroxyphenylalanine (l-Dopa) treatment in Parkinson's disease leads to involuntary movements called dyskinesia, notably through an overexpression of immediate-early genes (IEG). Their rapid transcription involves the stalling of RNA polymerase II on IEG promoters, a mechanism that critically depends on the presence of the negative elongation factor (NELF) protein complex. We here down-regulated the key NELF-E subunit using lentiviral vector delivery of a short hairpin RNA in the striatum of 6-hydroxydopamine lesioned rats. Such NELF-E reduced expression significantly attenuated the development of abnormal involuntary movements in response to chronic l-Dopa treatment. Effectiveness of silencing was demonstrated by the significant decrease in striatal ∆FosB, ARC and Zif268 IEG expression. Repression of NELF-mediating RNA polymerase II stalling thus achieves both antidyskinetic and potentiation of antiparkinsonian l-Dopa effect, highlighting the role of transcriptional events in dyskinesia establishment, acute dyskinetic manifestation and in the therapeutic response to l-Dopa.</abstract>
          </profileDesc>
        </hal>
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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Striatal NELF-mediated RNA polymerase II stalling controls l-dopa induced dyskinesia.

Striatal NELF-mediated RNA polymerase II stalling controls l-dopa induced dyskinesia.

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