Iron transport in Parkinson's disease.
Identifieur interne : 000B41 ( PubMed/Corpus ); précédent : 000B40; suivant : 000B42Iron transport in Parkinson's disease.
Auteurs : E C HirschSource :
- Parkinsonism & related disorders [ 1873-5126 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Cation Transport Proteins (genetics), Cation Transport Proteins (metabolism), Disease Models, Animal, Humans, Iron (metabolism), Mice, Neuroglia (metabolism), Oxidative Stress (physiology), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Substantia Nigra (metabolism), Substantia Nigra (pathology), Transferrin (metabolism).
- MESH :
- chemical , genetics : Cation Transport Proteins.
- chemical , metabolism : Cation Transport Proteins, Iron, Transferrin.
- genetics : Parkinson Disease.
- metabolism : Neuroglia, Parkinson Disease, Substantia Nigra.
- pathology : Parkinson Disease, Substantia Nigra.
- physiology : Oxidative Stress.
- physiopathology : Parkinson Disease.
- Animals, Disease Models, Animal, Humans, Mice.
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 neurons and glial cells in the SN of PD patients may contribute to the generation of oxidative stress, protein aggregation and neuronal death. However, the mechanisms involved in iron accumulation remain unclear. In previous studies we excluded a role of transferrin and its receptor in iron accumulation while we showed that lactoferrin receptors were overexpressed in blood vessels and dopaminergic neurons in Parkinson's disease. We recently also described an increase in the expression 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 increased in the ventral mesencephalon of intoxicated animals, concomitant with iron accumulation, oxidative stress and dopaminergic cell loss. A mutation in DMT1 that impairs iron transport protected rodents against parkinsonism-inducing neurotoxins MPTP and 6-hydroxydopamine (6-OHDA). This study supports a critical role for DMT1 in iron-mediated neurodegeneration in PD.
DOI: 10.1016/S1353-8020(09)70816-8
PubMed: 20082992
Links to Exploration step
pubmed:20082992Le document en format XML
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Iron accumulation in dopaminergic neurons and glial cells in the SN of PD patients may contribute to the generation of oxidative stress, protein aggregation and neuronal death. However, the mechanisms involved in iron accumulation remain unclear. In previous studies we excluded a role of transferrin and its receptor in iron accumulation while we showed that lactoferrin receptors were overexpressed in blood vessels and dopaminergic neurons in Parkinson's disease. We recently also described an increase in the expression 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 increased in the ventral mesencephalon of intoxicated animals, concomitant with iron accumulation, oxidative stress and dopaminergic cell loss. A mutation in DMT1 that impairs iron transport protected rodents against parkinsonism-inducing neurotoxins MPTP and 6-hydroxydopamine (6-OHDA). 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">20082992</PMID><DateCreated><Year>2010</Year><Month>01</Month><Day>19</Day></DateCreated><DateCompleted><Year>2010</Year><Month>03</Month><Day>31</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1873-5126</ISSN><JournalIssue CitedMedium="Internet"><Volume>15 Suppl 3</Volume><PubDate><Year>2009</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Parkinsonism & related disorders</Title><ISOAbbreviation>Parkinsonism Relat. Disord.</ISOAbbreviation></Journal><ArticleTitle>Iron transport in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>S209-11</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/S1353-8020(09)70816-8</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 neurons and glial cells in the SN of PD patients may contribute to the generation of oxidative stress, protein aggregation and neuronal death. However, the mechanisms involved in iron accumulation remain unclear. In previous studies we excluded a role of transferrin and its receptor in iron accumulation while we showed that lactoferrin receptors were overexpressed in blood vessels and dopaminergic neurons in Parkinson's disease. We recently also described an increase in the expression 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 increased in the ventral mesencephalon of intoxicated animals, concomitant with iron accumulation, oxidative stress and dopaminergic cell loss. A mutation in DMT1 that impairs iron transport protected rodents against parkinsonism-inducing neurotoxins MPTP and 6-hydroxydopamine (6-OHDA). This study supports a critical role for DMT1 in iron-mediated neurodegeneration in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials><AffiliationInfo><Affiliation>Université Pierre & Marie Curie-Paris 6, Centre de Recherche de l'Institut du Cerveau et de Moelle Epiniére , UMR-S975, Paris, France. etienne.hirsch@upmc.fr</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Parkinsonism Relat Disord</MedlineTA><NlmUniqueID>9513583</NlmUniqueID><ISSNLinking>1353-8020</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D027682">Cation Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014168">Transferrin</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></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D027682" MajorTopicYN="N">Cation Transport Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009457" MajorTopicYN="N">Neuroglia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014168" MajorTopicYN="N">Transferrin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>1</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>1</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>4</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20082992</ArticleId><ArticleId IdType="pii">S1353-8020(09)70816-8</ArticleId><ArticleId IdType="doi">10.1016/S1353-8020(09)70816-8</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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