Nigral overexpression of alpha-synuclein in the absence of parkin enhances alpha-synuclein phosphorylation but does not modulate dopaminergic neurodegeneration
Identifieur interne : 000561 ( Main/Exploration ); précédent : 000560; suivant : 000562Nigral overexpression of alpha-synuclein in the absence of parkin enhances alpha-synuclein phosphorylation but does not modulate dopaminergic neurodegeneration
Auteurs : Anne-Sophie Van Rompuy [Belgique] ; Marusela Oliveras-Salvá [Belgique] ; Anke Van Der Perren [Belgique] ; Olga Corti [France] ; Chris Van Den Haute [Belgique] ; Veerle Baekelandt [Belgique]Source :
- Molecular Neurodegeneration [ 1750-1326 ] ; 2015.
English descriptors
- mix :
Abstract
Alpha-synuclein is a key protein in the pathogenesis of Parkinson’s disease. Mutations in the parkin gene are the most common cause of early-onset autosomal recessive Parkinson’s disease, probably through a loss-of-function mechanism. However, the molecular mechanism by which loss of parkin function leads to the development of the disease and the role of alpha-synuclein in parkin-associated Parkinson’s disease is still not elucidated. Conflicting results were reported about the effect of the absence of parkin on alpha-synuclein-mediated neurotoxicity using a transgenic approach. In this study, we investigated the effect of loss of parkin on alpha-synuclein neuropathology and toxicity in adult rodent brain using viral vectors. Therefore, we overexpressed human wild type alpha-synuclein in the substantia nigra of parkin knockout and wild type mice using two different doses of recombinant adeno-associated viral vectors.
No difference was observed in nigral dopaminergic cell loss between the parkin knockout mice and wild type mice up to 16 weeks after viral vector injection. However, the level of alpha-synuclein phosphorylated at serine residue 129 in the substantia nigra was significantly increased in the parkin knockout mice compared to the wild type mice while the total expression level of alpha-synuclein was similar in both groups. The increased alpha-synuclein phosphorylation was confirmed in a parkin knockdown cell line.
These findings support a functional relationship between parkin and alpha-synuclein phosphorylation in rodent brain.
Url:
DOI: 10.1186/s13024-015-0017-8
PubMed: 26099628
PubMed Central: 4477319
Affiliations:
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Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation><affiliation wicri:level="3"><nlm:aff id="Aff4">CNRS, UMR 7225, F-75013 Paris, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>CNRS, UMR 7225, F-75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Van Den Haute, Chris" sort="Van Den Haute, Chris" uniqKey="Van Den Haute C" first="Chris" last="Van Den Haute">Chris Van Den Haute</name><affiliation wicri:level="1"><nlm:aff id="Aff1">Laboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders, Belgium</nlm:aff><country xml:lang="fr">Belgique</country><wicri:regionArea>Laboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders</wicri:regionArea><wicri:noRegion>Flanders</wicri:noRegion></affiliation><affiliation wicri:level="3"><nlm:aff id="Aff5">Leuven Viral Vector Core, KU Leuven, 3000 Leuven, Belgium</nlm:aff><country xml:lang="fr">Belgique</country><wicri:regionArea>Leuven Viral Vector Core, KU Leuven, 3000 Leuven</wicri:regionArea><placeName><region type="province" nuts="2">Province du Brabant flamand</region><settlement type="city">Louvain</settlement></placeName></affiliation></author><author><name sortKey="Baekelandt, Veerle" sort="Baekelandt, Veerle" uniqKey="Baekelandt V" first="Veerle" last="Baekelandt">Veerle Baekelandt</name><affiliation wicri:level="1"><nlm:aff id="Aff1">Laboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders, Belgium</nlm:aff><country xml:lang="fr">Belgique</country><wicri:regionArea>Laboratory for Neurobiology and Gene Therapy, Department of Neurosciences, KU Leuven, Flanders</wicri:regionArea><wicri:noRegion>Flanders</wicri:noRegion></affiliation></author></analytic><series><title level="j">Molecular Neurodegeneration</title><idno type="eISSN">1750-1326</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>Adeno-associated viral vectors</term><term>Alpha-synuclein</term><term>Alpha-synuclein phosphorylation</term><term>Knockout</term><term>Parkin</term><term>Parkinson's disease</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Alpha-synuclein is a key protein in the pathogenesis of Parkinson’s disease. Mutations in the parkin gene are the most common cause of early-onset autosomal recessive Parkinson’s disease, probably through a loss-of-function mechanism. However, the molecular mechanism by which loss of parkin function leads to the development of the disease and the role of alpha-synuclein in parkin-associated Parkinson’s disease is still not elucidated. Conflicting results were reported about the effect of the absence of parkin on alpha-synuclein-mediated neurotoxicity using a transgenic approach. In this study, we investigated the effect of loss of parkin on alpha-synuclein neuropathology and toxicity in adult rodent brain using viral vectors. Therefore, we overexpressed human wild type alpha-synuclein in the substantia nigra of parkin knockout and wild type mice using two different doses of recombinant adeno-associated viral vectors.</p></sec><sec><title>Results</title><p>No difference was observed in nigral dopaminergic cell loss between the parkin knockout mice and wild type mice up to 16 weeks after viral vector injection. However, the level of alpha-synuclein phosphorylated at serine residue 129 in the substantia nigra was significantly increased in the parkin knockout mice compared to the wild type mice while the total expression level of alpha-synuclein was similar in both groups. The increased alpha-synuclein phosphorylation was confirmed in a parkin knockdown cell line.</p></sec><sec><title>Conclusions</title><p>These findings support a functional relationship between parkin and alpha-synuclein phosphorylation in rodent brain.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Lees, Aj" uniqKey="Lees A">AJ Lees</name></author><author><name sortKey="Hardy, J" uniqKey="Hardy J">J Hardy</name></author><author><name sortKey="Revesz, T" uniqKey="Revesz T">T Revesz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schulte, C" uniqKey="Schulte C">C Schulte</name></author><author><name sortKey="Gasser, T" uniqKey="Gasser T">T Gasser</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Maroteaux, L" uniqKey="Maroteaux L">L Maroteaux</name></author><author><name sortKey="Campanelli, Jt" uniqKey="Campanelli J">JT 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sortKey="Hof, Pr" uniqKey="Hof P">PR Hof</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Osorio, L" uniqKey="Osorio L">L Osorio</name></author><author><name sortKey="Gijsbers, R" uniqKey="Gijsbers R">R Gijsbers</name></author><author><name sortKey="Oliveras Salva, M" uniqKey="Oliveras Salva M">M Oliveras-Salva</name></author><author><name sortKey="Michiels, A" uniqKey="Michiels A">A Michiels</name></author><author><name sortKey="Debyser, Z" uniqKey="Debyser Z">Z Debyser</name></author><author><name sortKey="Van Den Haute, C" uniqKey="Van Den Haute C">C Van den Haute</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Belgique</li><li>France</li></country><region><li>Province du Brabant flamand</li><li>Île-de-France</li></region><settlement><li>Louvain</li><li>Paris</li></settlement></list><tree><country name="Belgique"><noRegion><name sortKey="Van Rompuy, Anne Sophie" sort="Van Rompuy, Anne Sophie" uniqKey="Van Rompuy A" first="Anne-Sophie" last="Van Rompuy">Anne-Sophie Van Rompuy</name></noRegion><name sortKey="Baekelandt, Veerle" sort="Baekelandt, Veerle" uniqKey="Baekelandt V" first="Veerle" last="Baekelandt">Veerle Baekelandt</name><name sortKey="Oliveras Salva, Marusela" sort="Oliveras Salva, Marusela" uniqKey="Oliveras Salva M" first="Marusela" last="Oliveras-Salvá">Marusela Oliveras-Salvá</name><name sortKey="Van Den Haute, Chris" sort="Van Den Haute, Chris" uniqKey="Van Den Haute C" first="Chris" last="Van Den Haute">Chris Van Den Haute</name><name sortKey="Van Den Haute, Chris" sort="Van Den Haute, Chris" uniqKey="Van Den Haute C" first="Chris" last="Van Den Haute">Chris Van Den Haute</name><name sortKey="Van Der Perren, Anke" sort="Van Der Perren, Anke" uniqKey="Van Der Perren A" first="Anke" last="Van Der Perren">Anke Van Der Perren</name></country><country name="France"><region name="Île-de-France"><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name></region><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Nigral overexpression of alpha-synuclein in the absence of parkin enhances alpha-synuclein phosphorylation but does not modulate dopaminergic neurodegeneration
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