| Neuroprotection of α-synuclein under acute and chronic rotenone and maneb treatment is abolished by its familial Parkinson's disease mutations A30P, A53T and E46K. | |
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MedLine Citation:
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PMID: 21658409 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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α-Synuclein (α-Syn) plays a crucial role in the pathophysiology of Parkinson's disease (PD). α-Syn has been extensively studied in many neuronal cell-based PD models but has yielded mixed results. The objective of this study was to re-evaluate the dual cytotoxic/protective roles of α-Syn in dopaminergic SH-SY5Y cells. Stable SH-SY5Y cells overexpressing wild type or familial α-Syn mutants (A30P, E46K and A53T) were subjected to acute and chronic rotenone and maneb treatment. Compared with untransfected SH-SY5Y cells, wild type α-Syn attenuated rotenone and maneb-induced cell death along with an attenuation of toxin-induced mitochondrial membrane potential changes and Reactive Oxygen Species level, whereas the mutant α-Syn constructs exacerbated environmental toxins-induced cytotoxicity. After chronic treatment, wild type α-Syn but not the mutant variants was found to rescue cells from subsequent acute hydrogen peroxide insult. These results suggest that the fundamental property of wild type α-Syn may be protective, and such property may be lost by its familial PD mutations. |
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Authors:
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Chi-Jing Choong; Yee-How Say |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-5-30 |
Journal Detail:
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Title: Neurotoxicology Volume: - ISSN: 1872-9711 ISO Abbreviation: - Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-6-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7905589 Medline TA: Neurotoxicology Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011. Published by Elsevier B.V. |
Affiliation:
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Department of Biomedical Science, Faculty of Science, Universiti Tunku Abdul Rahman (UTAR) Perak Campus, 31900 Kampar, Perak, Malaysia. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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