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α-Synuclein Over-Expression Induces Increased Iron Accumulation and Redistribution in Iron-Exposed Neurons

hal.structure.identifierCentre d'Etudes Nucléaires de Bordeaux Gradignan [CENBG]
dc.contributor.authorORTEGA, Richard
hal.structure.identifierCentre d'Etudes Nucléaires de Bordeaux Gradignan [CENBG]
dc.contributor.authorCARMONA, Asuncion
hal.structure.identifierCentre d'Etudes Nucléaires de Bordeaux Gradignan [CENBG]
dc.contributor.authorROUDEAU, Stéphane
hal.structure.identifierCentre d'Etudes Nucléaires de Bordeaux Gradignan [CENBG]
dc.contributor.authorPERRIN, Laura
dc.contributor.authorDUČIĆ, Tanja
dc.contributor.authorCARBONI, Eleonora
dc.contributor.authorBOHIC, Sylvain
hal.structure.identifierEuropean Synchrotron Radiation Facility [ESRF]
dc.contributor.authorCLOETENS, Peter
dc.contributor.authorLINGOR, Paul
dc.date.issued2015
dc.description.abstractEnParkinson’s disease is the most common α-synucleinopathy, and increased levels of iron are found in the substantia nigra of Parkinson’s disease patients, but the potential interlink between both molecular changes has not been fully understood. Metal to protein binding assays have shown that α-synuclein can bind iron in vitro; therefore, we hypothesized that iron content and iron distribution could be modified in cellulo, in cells over-expressing α-synuclein. Owing to particle-induced X-ray emission and synchrotron X-ray fluorescence chemical nano-imaging, we were able to quantify and describe the iron distribution at the subcellular level. We show that, in neurons exposed to excess iron, the mere over-expression of human α-synuclein results in increased levels of intracellular iron and in iron redistribution from the cytoplasm to the perinuclear region within α-synuclein-rich inclusions. Reproducible results were obtained in two distinct recombinant expression systems, in primary rat midbrain neurons and in a rat neuroblastic cell line (PC12), both infected with viral vectors expressing human α-synuclein. Our results link two characteristic molecular features found in Parkinson’s disease, the accumulation of α-synuclein and the increased levels of iron in the substantia nigra.
dc.language.isoen
dc.title.enα-Synuclein Over-Expression Induces Increased Iron Accumulation and Redistribution in Iron-Exposed Neurons
dc.typeArticle de revue
dc.identifier.doi10.1007/s12035-015-9146-x
dc.subject.halPhysique [physics]
bordeaux.journalMolecular Neurobiology
bordeaux.page1925-1934
bordeaux.volume53
bordeaux.issue3
bordeaux.peerReviewedoui
hal.identifierhal-01758781
hal.version1
hal.popularnon
hal.audienceInternationale
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-01758781v1
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