G2019S-LRRK2 Expression Augments α-Synuclein Sequestration into Inclusions in Neurons.
Identifieur interne : 000347 ( Main/Exploration ); précédent : 000346; suivant : 000348G2019S-LRRK2 Expression Augments α-Synuclein Sequestration into Inclusions in Neurons.
Auteurs : Laura A. Volpicelli-Daley [États-Unis] ; Hisham Abdelmotilib [États-Unis] ; Zhiyong Liu [États-Unis] ; Lindsay Stoyka [États-Unis] ; João Paulo Lima Daher [États-Unis] ; Austen J. Milnerwood ; Vivek K. Unni [États-Unis] ; Warren D. Hirst [États-Unis] ; Zhenyu Yue [États-Unis] ; Hien T. Zhao ; Kyle Fraser [États-Unis] ; Richard E. Kennedy [États-Unis] ; Andrew B. West [États-Unis]Source :
- The Journal of neuroscience : the official journal of the Society for Neuroscience [ 1529-2401 ] ; 2016.
Abstract
Pathologic inclusions define α-synucleinopathies that include Parkinson's disease (PD). The most common genetic cause of PD is the G2019S LRRK2 mutation that upregulates LRRK2 kinase activity. However, the interaction between α-synuclein, LRRK2, and the formation of α-synuclein inclusions remains unclear. Here, we show that G2019S-LRRK2 expression, in both cultured neurons and dopaminergic neurons in the rat substantia nigra pars compact, increases the recruitment of endogenous α-synuclein into inclusions in response to α-synuclein fibril exposure. This results from the expression of mutant G2019S-LRRK2, as overexpression of WT-LRRK2 not only does not increase formation of inclusions but reduces their abundance. In addition, treatment of primary mouse neurons with LRRK2 kinase inhibitors, PF-06447475 and MLi-2, blocks G2019S-LRRK2 effects, suggesting that the G2019S-LRRK2 potentiation of inclusion formation depends on its kinase activity. Overexpression of G2019S-LRRK2 slightly increases, whereas WT-LRRK2 decreases, total levels of α-synuclein. Knockdown of total α-synuclein with potent antisense oligonucleotides substantially reduces inclusion formation in G2019S-LRRK2-expressing neurons, suggesting that LRRK2 influences α-synuclein inclusion formation by altering α-synuclein levels. These findings support the hypothesis that G2019S-LRRK2 may increase the progression of pathological α-synuclein inclusions after the initial formation of α-synuclein pathology by increasing a pool of α-synuclein that is more susceptible to forming inclusions.
DOI: 10.1523/JNEUROSCI.3642-15.2016
PubMed: 27413152
Affiliations:
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Volpicelli-Daley</name><affiliation wicri:level="1"><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294, volpicel@uab.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294</wicri:regionArea><wicri:noRegion>Alabama 35294</wicri:noRegion></affiliation></author><author><name sortKey="Abdelmotilib, Hisham" sort="Abdelmotilib, Hisham" uniqKey="Abdelmotilib H" first="Hisham" last="Abdelmotilib">Hisham Abdelmotilib</name><affiliation wicri:level="2"><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham</wicri:cityArea></affiliation></author><author><name sortKey="Liu, Zhiyong" sort="Liu, Zhiyong" uniqKey="Liu Z" first="Zhiyong" last="Liu">Zhiyong Liu</name><affiliation wicri:level="2"><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham</wicri:cityArea></affiliation></author><author><name sortKey="Stoyka, Lindsay" sort="Stoyka, Lindsay" uniqKey="Stoyka L" first="Lindsay" last="Stoyka">Lindsay Stoyka</name><affiliation wicri:level="2"><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham</wicri:cityArea></affiliation></author><author><name sortKey="Daher, Joao Paulo Lima" sort="Daher, Joao Paulo Lima" uniqKey="Daher J" first="João Paulo Lima" last="Daher">João Paulo Lima Daher</name><affiliation wicri:level="2"><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham</wicri:cityArea></affiliation></author><author><name sortKey="Milnerwood, Austen J" sort="Milnerwood, Austen J" uniqKey="Milnerwood A" first="Austen J" last="Milnerwood">Austen J. Milnerwood</name><affiliation><nlm:affiliation>Centre for Applied Neurogenetics, Medical Genetics, University of British Columbia, Vancouver, British Columbia, V6T 1Z3 Canada.</nlm:affiliation><wicri:noCountry code="subField">V6T 1Z3 Canada</wicri:noCountry></affiliation></author><author><name sortKey="Unni, Vivek K" sort="Unni, Vivek K" uniqKey="Unni V" first="Vivek K" last="Unni">Vivek K. Unni</name><affiliation wicri:level="2"><nlm:affiliation>Jungers Center for Neurosciences Research and Parkinson Center of Oregon, Department of Neurology, Oregon Health & Science University, Portland, Oregon 97239.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Oregon</region></placeName><wicri:cityArea>Jungers Center for Neurosciences Research and Parkinson Center of Oregon, Department of Neurology, Oregon Health & Science University, Portland</wicri:cityArea></affiliation></author><author><name sortKey="Hirst, Warren D" sort="Hirst, Warren D" uniqKey="Hirst W" first="Warren D" last="Hirst">Warren D. Hirst</name><affiliation wicri:level="2"><nlm:affiliation>Pfizer Neuroscience and Pain Research Unit, Cambridge, Massachusetts 02139.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Pfizer Neuroscience and Pain Research Unit, Cambridge</wicri:cityArea></affiliation></author><author><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name><affiliation wicri:level="2"><nlm:affiliation>Departments of Neurology and Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Departments of Neurology and Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York</wicri:cityArea></affiliation></author><author><name sortKey="Zhao, Hien T" sort="Zhao, Hien T" uniqKey="Zhao H" first="Hien T" last="Zhao">Hien T. Zhao</name><affiliation><nlm:affiliation>Ionis Pharmaceuticals, Carlsbad, California 92010, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Fraser, Kyle" sort="Fraser, Kyle" uniqKey="Fraser K" first="Kyle" last="Fraser">Kyle Fraser</name><affiliation wicri:level="2"><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham</wicri:cityArea></affiliation></author><author><name sortKey="Kennedy, Richard E" sort="Kennedy, Richard E" uniqKey="Kennedy R" first="Richard E" last="Kennedy">Richard E. Kennedy</name><affiliation wicri:level="2"><nlm:affiliation>Comprehensive Center for Healthy Aging and Division of Gerontology, Geriatrics, and Palliative Care, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Comprehensive Center for Healthy Aging and Division of Gerontology, Geriatrics, and Palliative Care, Department of Medicine, University of Alabama at Birmingham, Birmingham</wicri:cityArea></affiliation></author><author><name sortKey="West, Andrew B" sort="West, Andrew B" uniqKey="West A" first="Andrew B" last="West">Andrew B. West</name><affiliation wicri:level="2"><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Alabama</region></placeName><wicri:cityArea>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham</wicri:cityArea></affiliation></author></analytic><series><title level="j">The Journal of neuroscience : the official journal of the Society for Neuroscience</title><idno type="eISSN">1529-2401</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pathologic inclusions define α-synucleinopathies that include Parkinson's disease (PD). The most common genetic cause of PD is the G2019S LRRK2 mutation that upregulates LRRK2 kinase activity. However, the interaction between α-synuclein, LRRK2, and the formation of α-synuclein inclusions remains unclear. Here, we show that G2019S-LRRK2 expression, in both cultured neurons and dopaminergic neurons in the rat substantia nigra pars compact, increases the recruitment of endogenous α-synuclein into inclusions in response to α-synuclein fibril exposure. This results from the expression of mutant G2019S-LRRK2, as overexpression of WT-LRRK2 not only does not increase formation of inclusions but reduces their abundance. In addition, treatment of primary mouse neurons with LRRK2 kinase inhibitors, PF-06447475 and MLi-2, blocks G2019S-LRRK2 effects, suggesting that the G2019S-LRRK2 potentiation of inclusion formation depends on its kinase activity. Overexpression of G2019S-LRRK2 slightly increases, whereas WT-LRRK2 decreases, total levels of α-synuclein. Knockdown of total α-synuclein with potent antisense oligonucleotides substantially reduces inclusion formation in G2019S-LRRK2-expressing neurons, suggesting that LRRK2 influences α-synuclein inclusion formation by altering α-synuclein levels. These findings support the hypothesis that G2019S-LRRK2 may increase the progression of pathological α-synuclein inclusions after the initial formation of α-synuclein pathology by increasing a pool of α-synuclein that is more susceptible to forming inclusions.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Alabama</li><li>Massachusetts</li><li>Oregon</li><li>État de New York</li></region></list><tree><noCountry><name sortKey="Milnerwood, Austen J" sort="Milnerwood, Austen J" uniqKey="Milnerwood A" first="Austen J" last="Milnerwood">Austen J. Milnerwood</name><name sortKey="Zhao, Hien T" sort="Zhao, Hien T" uniqKey="Zhao H" first="Hien T" last="Zhao">Hien T. Zhao</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Volpicelli Daley, Laura A" sort="Volpicelli Daley, Laura A" uniqKey="Volpicelli Daley L" first="Laura A" last="Volpicelli-Daley">Laura A. Volpicelli-Daley</name></noRegion><name sortKey="Abdelmotilib, Hisham" sort="Abdelmotilib, Hisham" uniqKey="Abdelmotilib H" first="Hisham" last="Abdelmotilib">Hisham Abdelmotilib</name><name sortKey="Daher, Joao Paulo Lima" sort="Daher, Joao Paulo Lima" uniqKey="Daher J" first="João Paulo Lima" last="Daher">João Paulo Lima Daher</name><name sortKey="Fraser, Kyle" sort="Fraser, Kyle" uniqKey="Fraser K" first="Kyle" last="Fraser">Kyle Fraser</name><name sortKey="Hirst, Warren D" sort="Hirst, Warren D" uniqKey="Hirst W" first="Warren D" last="Hirst">Warren D. Hirst</name><name sortKey="Kennedy, Richard E" sort="Kennedy, Richard E" uniqKey="Kennedy R" first="Richard E" last="Kennedy">Richard E. Kennedy</name><name sortKey="Liu, Zhiyong" sort="Liu, Zhiyong" uniqKey="Liu Z" first="Zhiyong" last="Liu">Zhiyong Liu</name><name sortKey="Stoyka, Lindsay" sort="Stoyka, Lindsay" uniqKey="Stoyka L" first="Lindsay" last="Stoyka">Lindsay Stoyka</name><name sortKey="Unni, Vivek K" sort="Unni, Vivek K" uniqKey="Unni V" first="Vivek K" last="Unni">Vivek K. Unni</name><name sortKey="West, Andrew B" sort="West, Andrew B" uniqKey="West A" first="Andrew B" last="West">Andrew B. West</name><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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