ParkinsonFranceV1, Main, Exploration, bibRecordById, Hal:hal-01286252

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

Identifieur interne : 000382 ( Main/Exploration ); précédent : 000381; suivant : 000383

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

Affiliations:

Links toward previous steps (curation, corpus...)

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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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   |texte=   Striatal NELF-mediated RNA polymerase II stalling controls l-dopa induced dyskinesia.
}}

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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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