Divalent metal transporter 1 (DMT1) contributes to neurodegeneration in animal models of Parkinson's disease.
Identifieur interne : 000C07 ( PubMed/Curation ); précédent : 000C06; suivant : 000C08Divalent metal transporter 1 (DMT1) contributes to neurodegeneration in animal models of Parkinson's disease.
Auteurs : Julio Salazar [France] ; Natalia Mena ; Stephane Hunot ; Annick Prigent ; Daniel Alvarez-Fischer ; Miguel Arredondo ; Charles Duyckaerts ; Veronique Sazdovitch ; Lin Zhao ; Laura M. Garrick ; Marco T. Nu Ez ; Michael D. Garrick ; Rita Raisman-Vozari ; Etienne C. HirschSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2008.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine, Iron.
- chemical , physiology : Cation Transport Proteins.
- metabolism : Parkinson Disease.
- pathology : Parkinson Disease.
- physiopathology : Parkinson Disease.
- Aged, Aged, 80 and over, Animals, Disease Models, Animal, Humans, Mice, Oxidative Stress.
Abstract
Dopaminergic cell death in the substantia nigra (SN) is central to Parkinson's disease (PD), but the neurodegenerative mechanisms have not been completely elucidated. Iron accumulation in dopaminergic and glial cells in the SN of PD patients may contribute to the generation of oxidative stress, protein aggregation, and neuronal death. The mechanisms involved in iron accumulation also remain unclear. Here, we describe an increase in the expression of an isoform of the divalent metal transporter 1 (DMT1/Nramp2/Slc11a2) in the SN of PD patients. Using the PD animal model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication in mice, we showed that DMT1 expression increases in the ventral mesencephalon of intoxicated animals, concomitant with iron accumulation, oxidative stress, and dopaminergic cell loss. In addition, we report that a mutation in DMT1 that impairs iron transport protects rodents against parkinsonism-inducing neurotoxins MPTP and 6-hydroxydopamine. This study supports a critical role for DMT1 in iron-mediated neurodegeneration in PD.
DOI: 10.1073/pnas.0804373105
PubMed: 19011085
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Garrick</name></author><author><name sortKey="Nu Ez, Marco T" sort="Nu Ez, Marco T" uniqKey="Nu Ez M" first="Marco T" last="Nu Ez">Marco T. Nu Ez</name></author><author><name sortKey="Garrick, Michael D" sort="Garrick, Michael D" uniqKey="Garrick M" first="Michael D" last="Garrick">Michael D. Garrick</name></author><author><name sortKey="Raisman Vozari, Rita" sort="Raisman Vozari, Rita" uniqKey="Raisman Vozari R" first="Rita" last="Raisman-Vozari">Rita Raisman-Vozari</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Cation Transport Proteins (physiology)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Humans</term><term>Iron (metabolism)</term><term>Mice</term><term>Oxidative Stress</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Iron</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Cation Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term><term>Oxidative Stress</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dopaminergic cell death in the substantia nigra (SN) is central to Parkinson's disease (PD), but the neurodegenerative mechanisms have not been completely elucidated. Iron accumulation in dopaminergic and glial cells in the SN of PD patients may contribute to the generation of oxidative stress, protein aggregation, and neuronal death. The mechanisms involved in iron accumulation also remain unclear. Here, we describe an increase in the expression of an isoform of the divalent metal transporter 1 (DMT1/Nramp2/Slc11a2) in the SN of PD patients. Using the PD animal model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication in mice, we showed that DMT1 expression increases in the ventral mesencephalon of intoxicated animals, concomitant with iron accumulation, oxidative stress, and dopaminergic cell loss. In addition, we report that a mutation in DMT1 that impairs iron transport protects rodents against parkinsonism-inducing neurotoxins MPTP and 6-hydroxydopamine. This study supports a critical role for DMT1 in iron-mediated neurodegeneration in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19011085</PMID><DateCreated><Year>2008</Year><Month>11</Month><Day>26</Day></DateCreated><DateCompleted><Year>2009</Year><Month>01</Month><Day>07</Day></DateCompleted><DateRevised><Year>2014</Year><Month>09</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>105</Volume><Issue>47</Issue><PubDate><Year>2008</Year><Month>Nov</Month><Day>25</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>Divalent metal transporter 1 (DMT1) contributes to neurodegeneration in animal models of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>18578-83</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.0804373105</ELocationID><Abstract><AbstractText>Dopaminergic cell death in the substantia nigra (SN) is central to Parkinson's disease (PD), but the neurodegenerative mechanisms have not been completely elucidated. Iron accumulation in dopaminergic and glial cells in the SN of PD patients may contribute to the generation of oxidative stress, protein aggregation, and neuronal death. The mechanisms involved in iron accumulation also remain unclear. Here, we describe an increase in the expression of an isoform of the divalent metal transporter 1 (DMT1/Nramp2/Slc11a2) in the SN of PD patients. Using the PD animal model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication in mice, we showed that DMT1 expression increases in the ventral mesencephalon of intoxicated animals, concomitant with iron accumulation, oxidative stress, and dopaminergic cell loss. In addition, we report that a mutation in DMT1 that impairs iron transport protects rodents against parkinsonism-inducing neurotoxins MPTP and 6-hydroxydopamine. This study supports a critical role for DMT1 in iron-mediated neurodegeneration in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Salazar</LastName><ForeName>Julio</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institut National de la Santé et de la Recherche Médicale, Neurologie et Thérapeutique Expérimentale, Unité Mixte de Recherche S679, 47 Boulevard de l'Hôpital, 75013 Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mena</LastName><ForeName>Natalia</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Hunot</LastName><ForeName>Stephane</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Prigent</LastName><ForeName>Annick</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Alvarez-Fischer</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Arredondo</LastName><ForeName>Miguel</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Duyckaerts</LastName><ForeName>Charles</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Sazdovitch</LastName><ForeName>Veronique</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Lin</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Garrick</LastName><ForeName>Laura M</ForeName><Initials>LM</Initials></Author><Author ValidYN="Y"><LastName>Nuñez</LastName><ForeName>Marco T</ForeName><Initials>MT</Initials></Author><Author ValidYN="Y"><LastName>Garrick</LastName><ForeName>Michael D</ForeName><Initials>MD</Initials></Author><Author ValidYN="Y"><LastName>Raisman-Vozari</LastName><ForeName>Rita</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials></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>2008</Year><Month>11</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D027682">Cation Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C436204">solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Bioenerg Biomembr. 2004 Aug;36(4):375-9</RefSource><PMID Version="1">15377875</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2004 Jan;88(1):233-45</RefSource><PMID Version="1">14675167</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1967 May;17(5):427-42</RefSource><PMID Version="1">6067254</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1985 Jul;82(13):4553-7</RefSource><PMID Version="1">2989832</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 1988 Jul 28;334(6180):345-8</RefSource><PMID 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Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000503" 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HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i -Sk "pubmed:19011085" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
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