Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease.
Identifieur interne : 001235 ( PubMed/Curation ); précédent : 001234; suivant : 001236Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease.
Auteurs : Anne M. Landau [Canada] ; 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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<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>
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