The expression of DJ‐1 (PARK7) in normal human CNS and idiopathic Parkinson’s disease
Identifieur interne : 001564 ( Main/Exploration ); précédent : 001563; suivant : 001565The expression of DJ‐1 (PARK7) in normal human CNS and idiopathic Parkinson’s disease
Auteurs : Rina Bandopadhyay [Royaume-Uni] ; Ann E. Kingsbury [Royaume-Uni] ; Mark R. Cookson ; Andrew R. Reid ; Ian M. Evans ; Andrew D. Hope ; Alan M. Pittman ; Tammaryn Lashley ; Rosa Canet-Aviles ; David W. Miller ; Chris Mclendon ; Catherine Strand ; Andrew J. Leonard ; Patrick M. Abou-Sleiman ; Daniel G. Healy ; Hiroyashi Ariga ; Nicholas W. Wood ; Rohan De Silva ; Tamas Revesz ; John A. Hardy ; Andrew Lees (neurologue) [Royaume-Uni]Source :
- Brain [ 0006-8950 ] ; 2004-02.
English descriptors
- KwdEn :
- DA = dopaminergic; 2DGE = two‐dimensional gel electrophoresis; GFAP = glial fibrillary acidic protein; IR = immunoreactivity, immunoreactive; LB = Lewy body; LN =Lewy neurite; PSP = progressive supranuclear palsy; SN = substantia nigra, DJ‐1; Parkinson’s disease; immunohistochemistry; 2D gel electrophoresis; paraquat.
Abstract
Two mutations in the DJ‐1 gene on chromosome1p36 have been identified recently to cause early‐onset, autosomal recessive Parkinson’s disease. As no information is available regarding the distribution of DJ‐1 protein in the human brain, in this study we used a monoclonal antibody for DJ‐1 to map its distribution in frontal cortex and substantia nigra, regions invariably involved in Parkinson’s disease. Western blotting of human frontal cortex showed DJ‐1 to be an abundant protein in control, idiopathic Parkinson’s disease, cases with clinical and pathological phenotypes of Parkinson’s disease with R98Q polymorphism for DJ‐1, and in progressive supranuclear palsy (PSP) brains. We also showed that DJ‐1 immunoreactivity (IR) was particularly prominent in astrocytes and astrocytic processes in both control and Parkinson’s disease frontal cortex, whereas neurons showed light or no DJ‐1 IR. Only occasional Lewy bodies (LBs), the pathological hallmarks of Parkinson’s disease, showed faint DJ‐1 IR, localized to the outer halo. In preclinical studies we showed that DJ‐1 is expressed in primary hippocampal and astrocyte cultures of mouse brain. By 2D gel analysis we also showed multiple pI isoforms for DJ‐1 ranging between 5.5–6.6 in both control and Parkinson’s disease brains, whilst exposure of M17 cells to the oxidizing agent paraquat was manifested as a shift in pI of endogenous DJ‐1 towards more acidic isoforms. We conclude that DJ‐1 is not an essential component of LBs and Lewy neurites, is expressed mainly by astrocytes in human brain tissue and is sensitive to oxidative stress conditions. These results are consistent with the hypothesis that neuronal–glial interactions are important in the pathophysiology of Parkinson’s disease.
Url:
DOI: 10.1093/brain/awh054
Affiliations:
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Hardy</name><affiliation><wicri:noCountry code="syntax">???</wicri:noCountry></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name><affiliation><wicri:noCountry code="syntax">???</wicri:noCountry><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><orgName>National Hospital for Neurology and Neurosurgery</orgName></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain</title><title level="j" type="abbrev">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2004-02">2004-02</date><biblScope unit="volume">127</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="420">420</biblScope><biblScope unit="page" to="430">430</biblScope></imprint><idno type="ISSN">0006-8950</idno></series><idno type="istex">DA4BE02115489AC02CA2DEC2C405944536F3A03F</idno><idno type="DOI">10.1093/brain/awh054</idno><idno type="local">awh054</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DA = dopaminergic; 2DGE = two‐dimensional gel electrophoresis; GFAP = glial fibrillary acidic protein; IR = immunoreactivity, immunoreactive; LB = Lewy body; LN =Lewy neurite; PSP = progressive supranuclear palsy; SN = substantia nigra</term><term>DJ‐1; Parkinson’s disease; immunohistochemistry; 2D gel electrophoresis; paraquat</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Two mutations in the DJ‐1 gene on chromosome1p36 have been identified recently to cause early‐onset, autosomal recessive Parkinson’s disease. As no information is available regarding the distribution of DJ‐1 protein in the human brain, in this study we used a monoclonal antibody for DJ‐1 to map its distribution in frontal cortex and substantia nigra, regions invariably involved in Parkinson’s disease. Western blotting of human frontal cortex showed DJ‐1 to be an abundant protein in control, idiopathic Parkinson’s disease, cases with clinical and pathological phenotypes of Parkinson’s disease with R98Q polymorphism for DJ‐1, and in progressive supranuclear palsy (PSP) brains. We also showed that DJ‐1 immunoreactivity (IR) was particularly prominent in astrocytes and astrocytic processes in both control and Parkinson’s disease frontal cortex, whereas neurons showed light or no DJ‐1 IR. Only occasional Lewy bodies (LBs), the pathological hallmarks of Parkinson’s disease, showed faint DJ‐1 IR, localized to the outer halo. In preclinical studies we showed that DJ‐1 is expressed in primary hippocampal and astrocyte cultures of mouse brain. By 2D gel analysis we also showed multiple pI isoforms for DJ‐1 ranging between 5.5–6.6 in both control and Parkinson’s disease brains, whilst exposure of M17 cells to the oxidizing agent paraquat was manifested as a shift in pI of endogenous DJ‐1 towards more acidic isoforms. We conclude that DJ‐1 is not an essential component of LBs and Lewy neurites, is expressed mainly by astrocytes in human brain tissue and is sensitive to oxidative stress conditions. These results are consistent with the hypothesis that neuronal–glial interactions are important in the pathophysiology of Parkinson’s disease.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement><orgName><li>National Hospital for Neurology and Neurosurgery</li></orgName></list><tree><noCountry><name sortKey="Abou Leiman, Patrick M" sort="Abou Leiman, Patrick M" uniqKey="Abou Leiman P" first="Patrick M." last="Abou-Sleiman">Patrick M. Abou-Sleiman</name><name sortKey="Ariga, Hiroyashi" sort="Ariga, Hiroyashi" uniqKey="Ariga H" first="Hiroyashi" last="Ariga">Hiroyashi Ariga</name><name sortKey="Canet Viles, Rosa" sort="Canet Viles, Rosa" uniqKey="Canet Viles R" first="Rosa" last="Canet-Aviles">Rosa Canet-Aviles</name><name sortKey="Cookson, Mark R" sort="Cookson, Mark R" uniqKey="Cookson M" first="Mark R." last="Cookson">Mark R. Cookson</name><name sortKey="De Silva, Rohan" sort="De Silva, Rohan" uniqKey="De Silva R" first="Rohan" last="De Silva">Rohan De Silva</name><name sortKey="Evans, Ian M" sort="Evans, Ian M" uniqKey="Evans I" first="Ian M." last="Evans">Ian M. Evans</name><name sortKey="Hardy, John A" sort="Hardy, John A" uniqKey="Hardy J" first="John A." last="Hardy">John A. Hardy</name><name sortKey="Healy, Daniel G" sort="Healy, Daniel G" uniqKey="Healy D" first="Daniel G." last="Healy">Daniel G. Healy</name><name sortKey="Hope, Andrew D" sort="Hope, Andrew D" uniqKey="Hope A" first="Andrew D." last="Hope">Andrew D. Hope</name><name sortKey="Lashley, Tammaryn" sort="Lashley, Tammaryn" uniqKey="Lashley T" first="Tammaryn" last="Lashley">Tammaryn Lashley</name><name sortKey="Leonard, Andrew J" sort="Leonard, Andrew J" uniqKey="Leonard A" first="Andrew J." last="Leonard">Andrew J. Leonard</name><name sortKey="Mclendon, Chris" sort="Mclendon, Chris" uniqKey="Mclendon C" first="Chris" last="Mclendon">Chris Mclendon</name><name sortKey="Miller, David W" sort="Miller, David W" uniqKey="Miller D" first="David W." last="Miller">David W. Miller</name><name sortKey="Pittman, Alan M" sort="Pittman, Alan M" uniqKey="Pittman A" first="Alan M." last="Pittman">Alan M. Pittman</name><name sortKey="Reid, Andrew R" sort="Reid, Andrew R" uniqKey="Reid A" first="Andrew R." last="Reid">Andrew R. Reid</name><name sortKey="Revesz, Tamas" sort="Revesz, Tamas" uniqKey="Revesz T" first="Tamas" last="Revesz">Tamas Revesz</name><name sortKey="Strand, Catherine" sort="Strand, Catherine" uniqKey="Strand C" first="Catherine" last="Strand">Catherine Strand</name><name sortKey="Wood, Nicholas W" sort="Wood, Nicholas W" uniqKey="Wood N" first="Nicholas W." last="Wood">Nicholas W. Wood</name></noCountry><country name="Royaume-Uni"><noRegion><name sortKey="Bandopadhyay, Rina" sort="Bandopadhyay, Rina" uniqKey="Bandopadhyay R" first="Rina" last="Bandopadhyay">Rina Bandopadhyay</name></noRegion><name sortKey="Kingsbury, Ann E" sort="Kingsbury, Ann E" uniqKey="Kingsbury A" first="Ann E." last="Kingsbury">Ann E. Kingsbury</name><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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