Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease.
Identifieur interne : 000806 ( PubMed/Corpus ); précédent : 000805; suivant : 000807Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease.
Auteurs : Carmen Noelker ; Lydie Morel ; Thomas Lescot ; Anke Osterloh ; Daniel Alvarez-Fischer ; Minka Breloer ; Carmen Henze ; Candan Depboylu ; Delphine Skrzydelski ; Patrick P. Michel ; Richard C. Dodel ; Lixia Lu ; Etienne C. Hirsch ; Stéphane Hunot ; Andreas HartmannSource :
- Scientific reports [ 2045-2322 ] ; 2013.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Animals, Cell Death (genetics), Corpus Striatum (metabolism), Dopamine (metabolism), Homovanillic Acid (metabolism), Mice, Mice, Knockout, Microglia (metabolism), Parkinsonian Disorders (genetics), Parkinsonian Disorders (metabolism), Toll-Like Receptor 4 (genetics), Toll-Like Receptor 4 (metabolism).
- MESH :
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- genetics : Cell Death, Parkinsonian Disorders, Toll-Like Receptor 4.
- metabolism : Corpus Striatum, Dopamine, Homovanillic Acid, Microglia, Parkinsonian Disorders, Toll-Like Receptor 4.
- Animals, Mice, Mice, Knockout.
Abstract
In mammalians, toll-like receptors (TLR) signal-transduction pathways induce the expression of a variety of immune-response genes, including inflammatory cytokines. It is therefore plausible to assume that TLRs are mediators in glial cells triggering the release of cytokines that ultimately kill DA neurons in the substantia nigra in Parkinson disease (PD). Accordingly, recent data indicate that TLR4 is up-regulated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in a mouse model of PD. Here, we wished to evaluate the role of TLR4 in the acute mouse MPTP model of PD: TLR4-deficient mice and wild-type littermates control mice were used for the acute administration way of MPTP or a corresponding volume of saline. We demonstrate that TLR4-deficient mice are less vulnerable to MPTP intoxication than wild-type mice and display a decreased number of Iba1+ and MHC II+ activated microglial cells after MPTP application, suggesting that the TLR4 pathway is involved in experimental PD.
DOI: 10.1038/srep01393
PubMed: 23462811
Links to Exploration step
pubmed:23462811Le document en format XML
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Michel</name></author><author><name sortKey="Dodel, Richard C" sort="Dodel, Richard C" uniqKey="Dodel R" first="Richard C" last="Dodel">Richard C. Dodel</name></author><author><name sortKey="Lu, Lixia" sort="Lu, Lixia" uniqKey="Lu L" first="Lixia" last="Lu">Lixia Lu</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><author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name></author><author><name sortKey="Hartmann, Andreas" sort="Hartmann, Andreas" uniqKey="Hartmann A" first="Andreas" last="Hartmann">Andreas Hartmann</name></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects)</term><term>Animals</term><term>Cell Death (genetics)</term><term>Corpus Striatum (metabolism)</term><term>Dopamine (metabolism)</term><term>Homovanillic Acid (metabolism)</term><term>Mice</term><term>Mice, Knockout</term><term>Microglia (metabolism)</term><term>Parkinsonian Disorders (genetics)</term><term>Parkinsonian Disorders (metabolism)</term><term>Toll-Like Receptor 4 (genetics)</term><term>Toll-Like Receptor 4 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Death</term><term>Parkinsonian Disorders</term><term>Toll-Like Receptor 4</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Dopamine</term><term>Homovanillic Acid</term><term>Microglia</term><term>Parkinsonian Disorders</term><term>Toll-Like Receptor 4</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In mammalians, toll-like receptors (TLR) signal-transduction pathways induce the expression of a variety of immune-response genes, including inflammatory cytokines. It is therefore plausible to assume that TLRs are mediators in glial cells triggering the release of cytokines that ultimately kill DA neurons in the substantia nigra in Parkinson disease (PD). Accordingly, recent data indicate that TLR4 is up-regulated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in a mouse model of PD. Here, we wished to evaluate the role of TLR4 in the acute mouse MPTP model of PD: TLR4-deficient mice and wild-type littermates control mice were used for the acute administration way of MPTP or a corresponding volume of saline. We demonstrate that TLR4-deficient mice are less vulnerable to MPTP intoxication than wild-type mice and display a decreased number of Iba1+ and MHC II+ activated microglial cells after MPTP application, suggesting that the TLR4 pathway is involved in experimental PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23462811</PMID><DateCreated><Year>2013</Year><Month>03</Month><Day>06</Day></DateCreated><DateCompleted><Year>2013</Year><Month>08</Month><Day>22</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>3</Volume><PubDate><Year>2013</Year></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>1393</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/srep01393</ELocationID><Abstract><AbstractText>In mammalians, toll-like receptors (TLR) signal-transduction pathways induce the expression of a variety of immune-response genes, including inflammatory cytokines. It is therefore plausible to assume that TLRs are mediators in glial cells triggering the release of cytokines that ultimately kill DA neurons in the substantia nigra in Parkinson disease (PD). Accordingly, recent data indicate that TLR4 is up-regulated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in a mouse model of PD. Here, we wished to evaluate the role of TLR4 in the acute mouse MPTP model of PD: TLR4-deficient mice and wild-type littermates control mice were used for the acute administration way of MPTP or a corresponding volume of saline. We demonstrate that TLR4-deficient mice are less vulnerable to MPTP intoxication than wild-type mice and display a decreased number of Iba1+ and MHC II+ activated microglial cells after MPTP application, suggesting that the TLR4 pathway is involved in experimental PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Noelker</LastName><ForeName>Carmen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>INSERM UMR_S975, Université Pierre et Marie Curie Paris 06 UMR_S975, CNRS UMR 7225, CR-ICM, Groupe Hospitalier Pitié-Salpêtrière, 75013 Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morel</LastName><ForeName>Lydie</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Lescot</LastName><ForeName>Thomas</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Osterloh</LastName><ForeName>Anke</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Alvarez-Fischer</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Breloer</LastName><ForeName>Minka</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Henze</LastName><ForeName>Carmen</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Depboylu</LastName><ForeName>Candan</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Skrzydelski</LastName><ForeName>Delphine</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Michel</LastName><ForeName>Patrick P</ForeName><Initials>PP</Initials></Author><Author ValidYN="Y"><LastName>Dodel</LastName><ForeName>Richard C</ForeName><Initials>RC</Initials></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Lixia</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials></Author><Author ValidYN="Y"><LastName>Hunot</LastName><ForeName>Stéphane</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Hartmann</LastName><ForeName>Andreas</ForeName><Initials>A</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></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051197">Toll-Like Receptor 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>X77S6GMS36</RegistryNumber><NameOfSubstance UI="D006719">Homovanillic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2001 Jan;15(1):155-163</RefSource><PMID Version="1">11149903</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2012 Jan;18 Suppl 1:S17-20</RefSource><PMID Version="1">22166424</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1988 Aug;38(8):1285-91</RefSource><PMID Version="1">3399080</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1998 Dec 11;282(5396):2085-8</RefSource><PMID Version="1">9851930</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 1999 May 15;828(1-2):91-103</RefSource><PMID 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Jul;236(1-2):39-46</RefSource><PMID Version="1">21640391</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2011 Aug;179(2):954-63</RefSource><PMID Version="1">21801874</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neuroinflammation. 2011;8:137</RefSource><PMID Version="1">21989292</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 1988 Jul 28;334(6180):345-8</RefSource><PMID Version="1">2899295</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006719" MajorTopicYN="N">Homovanillic Acid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017628" MajorTopicYN="N">Microglia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020734" 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