Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease.
Identifieur interne : 001235 ( PubMed/Corpus ); précédent : 001234; suivant : 001236Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease.
Auteurs : Anne M. Landau ; Kelvin C. Luk ; Michelle-Lee Jones ; Rosmarie Siegrist-Johnstone ; Yoon Kow Young ; Edouard Kouassi ; Vladimir V. Rymar ; Alain Dagher ; Abbas F. Sadikot ; Julie DesbaratsSource :
- The Journal of experimental medicine [ 0022-1007 ] ; 2005.
English descriptors
- KwdEn :
- Aged, Animals, Antigens, CD95 (metabolism), Brain (pathology), Chromatography, High Pressure Liquid, Female, Flow Cytometry, Humans, Immunohistochemistry, Lymphoproliferative Disorders (metabolism), MPTP Poisoning (metabolism), Male, Mice, Mice, Mutant Strains, Middle Aged, Neurons (metabolism), Parkinson Disease (metabolism), Signal Transduction (physiology), Up-Regulation.
- MESH :
- chemical , metabolism : Antigens, CD95.
- metabolism : Lymphoproliferative Disorders, MPTP Poisoning, Neurons, Parkinson Disease.
- pathology : Brain.
- physiology : Signal Transduction.
- Aged, Animals, Chromatography, High Pressure Liquid, Female, Flow Cytometry, Humans, Immunohistochemistry, Male, Mice, Mice, Mutant Strains, Middle Aged, Up-Regulation.
Abstract
Fas (CD95), a member of the tumor necrosis factor-receptor superfamily, has been studied extensively as a death-inducing receptor in the immune system. However, Fas is also widely expressed in a number of other tissues, including in neurons. Here, we report that defects in the Fas/Fas ligand system unexpectedly render mice highly susceptible to neural degeneration in a model of Parkinson's disease. We found that Fas-deficient lymphoproliferative mice develop a dramatic phenotype resembling clinical Parkinson's disease, characterized by extensive nigrostriatal degeneration accompanied by tremor, hypokinesia, and loss of motor coordination, when treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at a dose that causes no neural degeneration or behavioral impairment in WT mice. Mice with generalized lymphoproliferative disease, which express a mutated Fas ligand, display an intermediate phenotype between that of lymphoproliferative and WT mice. Moreover, Fas engagement directly protects neuronal cells from MPTP/1-methyl-4-phenylpyridinium ion toxicity in vitro. Our data show that decreased Fas expression renders dopaminergic neurons highly susceptible to degeneration in response to a Parkinson-causing neurotoxin. These findings constitute the first evidence for a neuroprotective role for Fas in vivo.
DOI: 10.1084/jem.20050163
PubMed: 16129703
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pubmed:16129703Le document en format XML
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Luk</name></author><author><name sortKey="Jones, Michelle Lee" sort="Jones, Michelle Lee" uniqKey="Jones M" first="Michelle-Lee" last="Jones">Michelle-Lee Jones</name></author><author><name sortKey="Siegrist Johnstone, Rosmarie" sort="Siegrist Johnstone, Rosmarie" uniqKey="Siegrist Johnstone R" first="Rosmarie" last="Siegrist-Johnstone">Rosmarie Siegrist-Johnstone</name></author><author><name sortKey="Young, Yoon Kow" sort="Young, Yoon Kow" uniqKey="Young Y" first="Yoon Kow" last="Young">Yoon Kow Young</name></author><author><name sortKey="Kouassi, Edouard" sort="Kouassi, Edouard" uniqKey="Kouassi E" first="Edouard" last="Kouassi">Edouard Kouassi</name></author><author><name sortKey="Rymar, Vladimir V" sort="Rymar, Vladimir V" uniqKey="Rymar V" first="Vladimir V" last="Rymar">Vladimir V. Rymar</name></author><author><name sortKey="Dagher, Alain" sort="Dagher, Alain" uniqKey="Dagher A" first="Alain" last="Dagher">Alain Dagher</name></author><author><name sortKey="Sadikot, Abbas F" sort="Sadikot, Abbas F" uniqKey="Sadikot A" first="Abbas F" last="Sadikot">Abbas F. Sadikot</name></author><author><name sortKey="Desbarats, Julie" sort="Desbarats, Julie" uniqKey="Desbarats J" first="Julie" last="Desbarats">Julie Desbarats</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16129703</idno><idno type="pmid">16129703</idno><idno type="doi">10.1084/jem.20050163</idno><idno type="wicri:Area/PubMed/Corpus">001235</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001235</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease.</title><author><name sortKey="Landau, Anne M" sort="Landau, Anne M" uniqKey="Landau A" first="Anne M" last="Landau">Anne M. Landau</name><affiliation><nlm:affiliation>Department of Physiology, McGill University, Montreal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Luk, Kelvin C" sort="Luk, Kelvin C" uniqKey="Luk K" first="Kelvin C" last="Luk">Kelvin C. Luk</name></author><author><name sortKey="Jones, Michelle Lee" sort="Jones, Michelle Lee" uniqKey="Jones M" first="Michelle-Lee" last="Jones">Michelle-Lee Jones</name></author><author><name sortKey="Siegrist Johnstone, Rosmarie" sort="Siegrist Johnstone, Rosmarie" uniqKey="Siegrist Johnstone R" first="Rosmarie" last="Siegrist-Johnstone">Rosmarie Siegrist-Johnstone</name></author><author><name sortKey="Young, Yoon Kow" sort="Young, Yoon Kow" uniqKey="Young Y" first="Yoon Kow" last="Young">Yoon Kow Young</name></author><author><name sortKey="Kouassi, Edouard" sort="Kouassi, Edouard" uniqKey="Kouassi E" first="Edouard" last="Kouassi">Edouard Kouassi</name></author><author><name sortKey="Rymar, Vladimir V" sort="Rymar, Vladimir V" uniqKey="Rymar V" first="Vladimir V" last="Rymar">Vladimir V. Rymar</name></author><author><name sortKey="Dagher, Alain" sort="Dagher, Alain" uniqKey="Dagher A" first="Alain" last="Dagher">Alain Dagher</name></author><author><name sortKey="Sadikot, Abbas F" sort="Sadikot, Abbas F" uniqKey="Sadikot A" first="Abbas F" last="Sadikot">Abbas F. Sadikot</name></author><author><name sortKey="Desbarats, Julie" sort="Desbarats, Julie" uniqKey="Desbarats J" first="Julie" last="Desbarats">Julie Desbarats</name></author></analytic><series><title level="j">The Journal of experimental medicine</title><idno type="ISSN">0022-1007</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Animals</term><term>Antigens, CD95 (metabolism)</term><term>Brain (pathology)</term><term>Chromatography, High Pressure Liquid</term><term>Female</term><term>Flow Cytometry</term><term>Humans</term><term>Immunohistochemistry</term><term>Lymphoproliferative Disorders (metabolism)</term><term>MPTP Poisoning (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Mutant Strains</term><term>Middle Aged</term><term>Neurons (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Signal Transduction (physiology)</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, CD95</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lymphoproliferative Disorders</term><term>MPTP Poisoning</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Animals</term><term>Chromatography, High Pressure Liquid</term><term>Female</term><term>Flow Cytometry</term><term>Humans</term><term>Immunohistochemistry</term><term>Male</term><term>Mice</term><term>Mice, Mutant Strains</term><term>Middle Aged</term><term>Up-Regulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fas (CD95), a member of the tumor necrosis factor-receptor superfamily, has been studied extensively as a death-inducing receptor in the immune system. However, Fas is also widely expressed in a number of other tissues, including in neurons. Here, we report that defects in the Fas/Fas ligand system unexpectedly render mice highly susceptible to neural degeneration in a model of Parkinson's disease. We found that Fas-deficient lymphoproliferative mice develop a dramatic phenotype resembling clinical Parkinson's disease, characterized by extensive nigrostriatal degeneration accompanied by tremor, hypokinesia, and loss of motor coordination, when treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at a dose that causes no neural degeneration or behavioral impairment in WT mice. Mice with generalized lymphoproliferative disease, which express a mutated Fas ligand, display an intermediate phenotype between that of lymphoproliferative and WT mice. Moreover, Fas engagement directly protects neuronal cells from MPTP/1-methyl-4-phenylpyridinium ion toxicity in vitro. Our data show that decreased Fas expression renders dopaminergic neurons highly susceptible to degeneration in response to a Parkinson-causing neurotoxin. These findings constitute the first evidence for a neuroprotective role for Fas in vivo.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16129703</PMID><DateCreated><Year>2005</Year><Month>09</Month><Day>08</Day></DateCreated><DateCompleted><Year>2006</Year><Month>02</Month><Day>27</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0022-1007</ISSN><JournalIssue CitedMedium="Print"><Volume>202</Volume><Issue>5</Issue><PubDate><Year>2005</Year><Month>Sep</Month><Day>05</Day></PubDate></JournalIssue><Title>The Journal of experimental medicine</Title><ISOAbbreviation>J. Exp. Med.</ISOAbbreviation></Journal><ArticleTitle>Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>575-81</MedlinePgn></Pagination><Abstract><AbstractText>Fas (CD95), a member of the tumor necrosis factor-receptor superfamily, has been studied extensively as a death-inducing receptor in the immune system. However, Fas is also widely expressed in a number of other tissues, including in neurons. Here, we report that defects in the Fas/Fas ligand system unexpectedly render mice highly susceptible to neural degeneration in a model of Parkinson's disease. We found that Fas-deficient lymphoproliferative mice develop a dramatic phenotype resembling clinical Parkinson's disease, characterized by extensive nigrostriatal degeneration accompanied by tremor, hypokinesia, and loss of motor coordination, when treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at a dose that causes no neural degeneration or behavioral impairment in WT mice. Mice with generalized lymphoproliferative disease, which express a mutated Fas ligand, display an intermediate phenotype between that of lymphoproliferative and WT mice. Moreover, Fas engagement directly protects neuronal cells from MPTP/1-methyl-4-phenylpyridinium ion toxicity in vitro. Our data show that decreased Fas expression renders dopaminergic neurons highly susceptible to degeneration in response to a Parkinson-causing neurotoxin. These findings constitute the first evidence for a neuroprotective role for Fas in vivo.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Landau</LastName><ForeName>Anne M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Physiology, McGill University, Montreal, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luk</LastName><ForeName>Kelvin C</ForeName><Initials>KC</Initials></Author><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>Michelle-Lee</ForeName><Initials>ML</Initials></Author><Author ValidYN="Y"><LastName>Siegrist-Johnstone</LastName><ForeName>Rosmarie</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Yoon Kow</ForeName><Initials>YK</Initials></Author><Author ValidYN="Y"><LastName>Kouassi</LastName><ForeName>Edouard</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Rymar</LastName><ForeName>Vladimir V</ForeName><Initials>VV</Initials></Author><Author ValidYN="Y"><LastName>Dagher</LastName><ForeName>Alain</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Sadikot</LastName><ForeName>Abbas F</ForeName><Initials>AF</Initials></Author><Author ValidYN="Y"><LastName>Desbarats</LastName><ForeName>Julie</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R21 NS4377353337</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>08</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Exp Med</MedlineTA><NlmUniqueID>2985109R</NlmUniqueID><ISSNLinking>0022-1007</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019014">Antigens, CD95</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Cell Biol. 1999 Nov 29;147(5):1049-62</RefSource><PMID Version="1">10579724</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2004 Nov 18;44(4):575-7</RefSource><PMID Version="1">15541303</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci Res. 2001 Mar 1;63(5):421-8</RefSource><PMID Version="1">11223917</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroscience. 2001;106(3):589-601</RefSource><PMID Version="1">11591459</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res Brain Res Protoc. 2002 Apr;9(2):105-11</RefSource><PMID Version="1">12034329</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2002 Sep 12;35(6):1067-83</RefSource><PMID Version="1">12354397</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Cell Biol. 2003 Feb;5(2):118-25</RefSource><PMID Version="1">12545171</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Development. 2003 Jun;130(11):2535-42</RefSource><PMID Version="1">12702666</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Neurosci. 2003 May;4(5):365-75</RefSource><PMID Version="1">12728264</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2003 Sep 11;39(6):889-909</RefSource><PMID Version="1">12971891</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res Brain Res Rev. 2004 Jan;44(1):65-81</RefSource><PMID Version="1">14739003</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Immunol. 2004 Feb 15;172(4):2118-25</RefSource><PMID Version="1">14764677</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2004 Feb 25;24(8):2045-53</RefSource><PMID Version="1">14985447</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Toxicol Lett. 2004 Apr 1;149(1-3):59-66</RefSource><PMID Version="1">15093249</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1992 Jun;42(6):1142-6</RefSource><PMID Version="1">1603339</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1992;32 Suppl:S125-7</RefSource><PMID Version="1">1510370</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1993 Mar 1;90(5):1756-60</RefSource><PMID Version="1">7680478</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 1994 Mar 25;76(6):969-76</RefSource><PMID Version="1">7511063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 1995 Nov;11(3):294-300</RefSource><PMID Version="1">7581453</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1996 May 14;93(10):4565-71</RefSource><PMID Version="1">8643444</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 1996 Dec 20;220(3):195-8</RefSource><PMID Version="1">8994226</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 1997 Feb 7;88(3):355-65</RefSource><PMID Version="1">9039262</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1998 Sep;44(3):425-6</RefSource><PMID Version="1">9749619</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1999 Jan 15;19(2):664-73</RefSource><PMID Version="1">9880587</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1999 May 15;19(10):3809-17</RefSource><PMID Version="1">10234013</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropathol Appl Neurobiol. 2000 Oct;26(5):424-33</RefSource><PMID Version="1">11054182</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019014" MajorTopicYN="N">Antigens, CD95</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002851" MajorTopicYN="N">Chromatography, High Pressure Liquid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008232" MajorTopicYN="N">Lymphoproliferative Disorders</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020267" 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