Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease
Identifieur interne : 000336 ( Pmc/Curation ); précédent : 000335; suivant : 000337Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease
Auteurs : Anne M. Landau [Canada] ; Kelvin C. Luk [Canada] ; Michelle-Lee Jones [Canada] ; Rosmarie Siegrist-Johnstone [Canada] ; Yoon Kow Young [Canada] ; Edouard Kouassi ; Vladimir V. Rymar [Canada] ; Alain Dagher [Canada] ; Abbas F. Sadikot [Canada] ; Julie Desbarats [Canada]Source :
- The Journal of Experimental Medicine [ 0022-1007 ] ; 2005.
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.
Url:
DOI: 10.1084/jem.20050163
PubMed: 16129703
PubMed Central: 2212882
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Edouard Kouassi<affiliation><nlm:aff id="aff4">Guy-Bernier Research Center, Maisonneuve-Rosemont Hospital</nlm:aff>
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<affiliation><nlm:aff id="aff5">Department of Medicine, University of Montreal, Montreal, Quebec, Canada, H1T 2M4</nlm:aff>
<wicri:noCountry code="subfield">H1T 2M4</wicri:noCountry>
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<affiliation><nlm:aff id="aff5">Department of Medicine, University of Montreal, Montreal, Quebec, Canada, H1T 2M4</nlm:aff>
<wicri:noCountry code="subfield">H1T 2M4</wicri:noCountry>
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<front><div type="abstract" xml:lang="en"><p>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.</p>
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<journal-title>The Journal of Experimental Medicine</journal-title>
<issn pub-type="ppub">0022-1007</issn>
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<title-group><article-title>Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Landau</surname>
<given-names>Anne M.</given-names>
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<contrib contrib-type="author"><name><surname>Luk</surname>
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<contrib contrib-type="author"><name><surname>Siegrist-Johnstone</surname>
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<contrib contrib-type="author"><name><surname>Kouassi</surname>
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<contrib contrib-type="author"><name><surname>Rymar</surname>
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<aff id="aff1"><label>1</label>
Department of Physiology, McGill University, Montreal, Quebec, Canada, H3G 1Y6</aff>
<aff id="aff2"><label>2</label>
Division of Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada, H3A 2B4</aff>
<aff id="aff3"><label>3</label>
McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada, H3A 2B4</aff>
<aff id="aff4"><label>4</label>
Guy-Bernier Research Center, Maisonneuve-Rosemont Hospital</aff>
<aff id="aff5"><label>5</label>
Department of Medicine, University of Montreal, Montreal, Quebec, Canada, H1T 2M4</aff>
<author-notes><fn><p>CORRESPONDENCE Julie Desbarats: <email>Julie.desbarats@mcgill.ca</email>
</p>
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<pub-date pub-type="ppub"><day>5</day>
<month>9</month>
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<issue>5</issue>
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<month>1</month>
<year>2005</year>
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<date date-type="accepted"><day>13</day>
<month>7</month>
<year>2005</year>
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<permissions><copyright-statement>Copyright © 2005, The Rockefeller University Press</copyright-statement>
</permissions>
<abstract><p>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.</p>
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