Glutaredoxin 1 Downregulation in the Substantia Nigra Leads to Dopaminergic Degeneration in Mice.
Identifieur interne : 000070 ( Main/Exploration ); précédent : 000069; suivant : 000071Glutaredoxin 1 Downregulation in the Substantia Nigra Leads to Dopaminergic Degeneration in Mice.
Auteurs : Aditi Verma [Inde] ; Ajit Ray [Inde] ; Deepti Bapat [Inde] ; Latha Diwakar [Inde] ; Reddy Peera Kommaddi [Inde] ; Bernard L. Schneider [Suisse] ; Etienne C. Hirsch [France] ; Vijayalakshmi Ravindranath [Inde]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2020.
Abstract
BACKGROUND
Parkinson's disease (PD) is characterized by a severe loss of the dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Perturbation of protein thiol redox homeostasis has been shown to play a role in the dysregulation of cell death and cell survival signaling pathways in these neurons. Glutaredoxin 1 (Grx1) is a thiol/disulfide oxidoreductase that catalyzes the deglutathionylation of proteins and is important for regulation of cellular protein thiol redox homeostasis.
OBJECTIVES
We evaluated if the downregulation of Grx1 could lead to dopaminergic degeneration and PD-relevant motor deficits in mice.
METHODS
Grx1 was downregulated unilaterally through viral vector-mediated transduction of short hairpin RNA against Grx1 into the SNpc. Behavioral assessment was performed through rotarod and elevated body swing test. Stereological analysis of tyrosine hydroxylase-positive and Nissl-positive neurons was carried out to evaluate neurodegeneration.
RESULTS
Downregulation of Grx1 resulted in contralateral bias of elevated body swing and reduced latency to fall off, accelerating rotarod. This was accompanied by a loss of tyrosine hydroxylase-positive neurons in the SNpc and their DA projections in the striatum. Furthermore, there was a loss Nissl-positive neurons in the SNpc, indicating cell death. This was selective to the SNpc neurons because DA neurons in the ventral tegmental area were unaffected akin to that seen in human PD. Furthermore, Grx1 mRNA expression was substantially decreased in the SNpc from PD patients.
CONCLUSIONS
Our study indicates that Grx1 is critical for the survival of SNpc DA neurons and that it is downregulated in human PD. © 2020 International Parkinson and Movement Disorder Society.
DOI: 10.1002/mds.28190
PubMed: 32618039
Affiliations:
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Schneider</name><affiliation wicri:level="1"><nlm:affiliation>Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne</wicri:regionArea><wicri:noRegion>CH-1015 Lausanne</wicri:noRegion></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="3"><nlm:affiliation>Institut du Cerveau-ICM Inserm U 1127, CNRS UMR 7225, Sorbonne Université, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Institut du Cerveau-ICM Inserm U 1127, CNRS UMR 7225, Sorbonne Université, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Ravindranath, Vijayalakshmi" sort="Ravindranath, Vijayalakshmi" uniqKey="Ravindranath V" first="Vijayalakshmi" last="Ravindranath">Vijayalakshmi Ravindranath</name><affiliation wicri:level="1"><nlm:affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Neuroscience, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Centre for Brain Research, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Brain Research, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32618039</idno><idno type="pmid">32618039</idno><idno type="doi">10.1002/mds.28190</idno><idno type="wicri:Area/Main/Corpus">000041</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000041</idno><idno type="wicri:Area/Main/Curation">000041</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000041</idno><idno 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Neuroscience, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation></author><author><name sortKey="Bapat, Deepti" sort="Bapat, Deepti" uniqKey="Bapat D" first="Deepti" last="Bapat">Deepti Bapat</name><affiliation wicri:level="1"><nlm:affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Neuroscience, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation></author><author><name sortKey="Diwakar, Latha" sort="Diwakar, Latha" uniqKey="Diwakar L" first="Latha" last="Diwakar">Latha Diwakar</name><affiliation wicri:level="1"><nlm:affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Neuroscience, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Centre for Brain Research, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Brain Research, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation></author><author><name sortKey="Kommaddi, Reddy Peera" sort="Kommaddi, Reddy Peera" uniqKey="Kommaddi R" first="Reddy Peera" last="Kommaddi">Reddy Peera Kommaddi</name><affiliation wicri:level="1"><nlm:affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Neuroscience, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Centre for Brain Research, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Brain Research, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation></author><author><name sortKey="Schneider, Bernard L" sort="Schneider, Bernard L" uniqKey="Schneider B" first="Bernard L" last="Schneider">Bernard L. Schneider</name><affiliation wicri:level="1"><nlm:affiliation>Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne</wicri:regionArea><wicri:noRegion>CH-1015 Lausanne</wicri:noRegion></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="3"><nlm:affiliation>Institut du Cerveau-ICM Inserm U 1127, CNRS UMR 7225, Sorbonne Université, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Institut du Cerveau-ICM Inserm U 1127, CNRS UMR 7225, Sorbonne Université, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Ravindranath, Vijayalakshmi" sort="Ravindranath, Vijayalakshmi" uniqKey="Ravindranath V" first="Vijayalakshmi" last="Ravindranath">Vijayalakshmi Ravindranath</name><affiliation wicri:level="1"><nlm:affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Neuroscience, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Centre for Brain Research, Indian Institute of Science, Bangalore, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Centre for Brain Research, Indian Institute of Science, Bangalore</wicri:regionArea><wicri:noRegion>Bangalore</wicri:noRegion></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>Parkinson's disease (PD) is characterized by a severe loss of the dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Perturbation of protein thiol redox homeostasis has been shown to play a role in the dysregulation of cell death and cell survival signaling pathways in these neurons. Glutaredoxin 1 (Grx1) is a thiol/disulfide oxidoreductase that catalyzes the deglutathionylation of proteins and is important for regulation of cellular protein thiol redox homeostasis.</p></div><div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b></p><p>We evaluated if the downregulation of Grx1 could lead to dopaminergic degeneration and PD-relevant motor deficits in mice.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>Grx1 was downregulated unilaterally through viral vector-mediated transduction of short hairpin RNA against Grx1 into the SNpc. Behavioral assessment was performed through rotarod and elevated body swing test. Stereological analysis of tyrosine hydroxylase-positive and Nissl-positive neurons was carried out to evaluate neurodegeneration.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>Downregulation of Grx1 resulted in contralateral bias of elevated body swing and reduced latency to fall off, accelerating rotarod. This was accompanied by a loss of tyrosine hydroxylase-positive neurons in the SNpc and their DA projections in the striatum. Furthermore, there was a loss Nissl-positive neurons in the SNpc, indicating cell death. This was selective to the SNpc neurons because DA neurons in the ventral tegmental area were unaffected akin to that seen in human PD. Furthermore, Grx1 mRNA expression was substantially decreased in the SNpc from PD patients.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Our study indicates that Grx1 is critical for the survival of SNpc DA neurons and that it is downregulated in human PD. © 2020 International Parkinson and Movement Disorder Society.</p></div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32618039</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>35</Volume><Issue>10</Issue><PubDate><Year>2020</Year><Month>10</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov Disord</ISOAbbreviation></Journal><ArticleTitle>Glutaredoxin 1 Downregulation in the Substantia Nigra Leads to Dopaminergic Degeneration in Mice.</ArticleTitle><Pagination><MedlinePgn>1843-1853</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.28190</ELocationID><Abstract><AbstractText Label="BACKGROUND">Parkinson's disease (PD) is characterized by a severe loss of the dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Perturbation of protein thiol redox homeostasis has been shown to play a role in the dysregulation of cell death and cell survival signaling pathways in these neurons. Glutaredoxin 1 (Grx1) is a thiol/disulfide oxidoreductase that catalyzes the deglutathionylation of proteins and is important for regulation of cellular protein thiol redox homeostasis.</AbstractText><AbstractText Label="OBJECTIVES">We evaluated if the downregulation of Grx1 could lead to dopaminergic degeneration and PD-relevant motor deficits in mice.</AbstractText><AbstractText Label="METHODS">Grx1 was downregulated unilaterally through viral vector-mediated transduction of short hairpin RNA against Grx1 into the SNpc. Behavioral assessment was performed through rotarod and elevated body swing test. Stereological analysis of tyrosine hydroxylase-positive and Nissl-positive neurons was carried out to evaluate neurodegeneration.</AbstractText><AbstractText Label="RESULTS">Downregulation of Grx1 resulted in contralateral bias of elevated body swing and reduced latency to fall off, accelerating rotarod. This was accompanied by a loss of tyrosine hydroxylase-positive neurons in the SNpc and their DA projections in the striatum. Furthermore, there was a loss Nissl-positive neurons in the SNpc, indicating cell death. This was selective to the SNpc neurons because DA neurons in the ventral tegmental area were unaffected akin to that seen in human PD. Furthermore, Grx1 mRNA expression was substantially decreased in the SNpc from PD patients.</AbstractText><AbstractText Label="CONCLUSIONS">Our study indicates that Grx1 is critical for the survival of SNpc DA neurons and that it is downregulated in human PD. © 2020 International Parkinson and Movement Disorder Society.</AbstractText><CopyrightInformation>© 2020 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Verma</LastName><ForeName>Aditi</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ray</LastName><ForeName>Ajit</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bapat</LastName><ForeName>Deepti</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Diwakar</LastName><ForeName>Latha</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centre for Brain Research, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kommaddi</LastName><ForeName>Reddy Peera</ForeName><Initials>RP</Initials><AffiliationInfo><Affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centre for Brain Research, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schneider</LastName><ForeName>Bernard L</ForeName><Initials>BL</Initials><AffiliationInfo><Affiliation>Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials><Identifier Source="ORCID">0000-0003-4823-276X</Identifier><AffiliationInfo><Affiliation>Institut du Cerveau-ICM Inserm U 1127, CNRS UMR 7225, Sorbonne Université, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ravindranath</LastName><ForeName>Vijayalakshmi</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0003-3226-0782</Identifier><AffiliationInfo><Affiliation>Centre for Neuroscience, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Centre for Brain Research, Indian Institute of Science, Bangalore, India.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>07</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Parkinson's disease</Keyword><Keyword MajorTopicYN="Y">dopaminergic neurons</Keyword><Keyword MajorTopicYN="Y">glutaredoxin 1</Keyword><Keyword MajorTopicYN="Y">shRNA</Keyword><Keyword MajorTopicYN="Y">tyrosine hydroxylase</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>09</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>06</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>06</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32618039</ArticleId><ArticleId IdType="doi">10.1002/mds.28190</ArticleId></ArticleIdList><ReferenceList><Title>References</Title><Reference><Citation>Schapira AHV, Cooper JM, Dexter D, Clark JB, Jenner P, Marsden CD. 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Schneider</name></noRegion></country><country name="France"><region name="Île-de-France"><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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