Abstract
Striatal mitochondrial proteins were investigated using proteomics in the 1-methyl 4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. Four proteins, 19S proteasome ATPase Rpt6 (19S Rpt6), Lectin-related nature killer cell receptor LY 49S, Zinc finger A20 domain containing 1, and the sodium channel-associated protein 1 isoform 2, were significantly decreased while alpha-synuclein was increased in MPTP-treated mice. The altered levels of 19S Rpt6 and alpha-synuclein were further verified by Western blot. Experiments using small interfering RNA (siRNA) showed that alpha-synuclein was increased by 50% in cultured striatal neurons when 19S Rpt6 was knocked down. Taken together, our results imply that a deficiency in 19S Rpt6 may be partially related to the MPTP-induced increase in alpha-synuclein in the striatum.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / pharmacology
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Adenosine Triphosphatases / genetics
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Adenosine Triphosphatases / metabolism*
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Animals
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Antigens, Ly / metabolism
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Corpus Striatum / drug effects
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Corpus Striatum / metabolism*
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Corpus Striatum / pathology
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Lectins, C-Type / metabolism
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Male
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Mice
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Mice, Inbred C57BL
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Neurons / drug effects
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Neurons / metabolism
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Neurons / pathology
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Neurotoxins / toxicity
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Parkinson Disease, Secondary / chemically induced
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Parkinson Disease, Secondary / genetics
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Parkinson Disease, Secondary / metabolism*
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Proteomics
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RNA Interference
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Receptors, NK Cell Lectin-Like
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alpha-Synuclein / metabolism*
Substances
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Antigens, Ly
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Lectins, C-Type
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Neurotoxins
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Receptors, NK Cell Lectin-Like
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alpha-Synuclein
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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
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Adenosine Triphosphatases