1-methyl-4-phenylpyridinium neurotoxicity is attenuated by adenoviral gene transfer of human Cu/Zn superoxide dismutase.
Identifieur interne : 000E47 ( PubMed/Curation ); précédent : 000E46; suivant : 000E481-methyl-4-phenylpyridinium neurotoxicity is attenuated by adenoviral gene transfer of human Cu/Zn superoxide dismutase.
Auteurs : Martine Barkats [France] ; Philippe Horellou ; Philippe Colin ; Stéphanie Millecamps ; Nicole Faucon-Biguet ; Jacques MalletSource :
- Journal of neuroscience research [ 0360-4012 ] ; 2006.
English descriptors
- KwdEn :
- 1-Methyl-4-phenylpyridinium (toxicity), Animals, Cell Count (methods), Cell Line, Tumor, Disease Models, Animal, Female, Gene Transfer Techniques, Genetic Therapy (methods), Genetic Vectors (physiology), Humans, Immunohistochemistry (methods), Motor Activity (physiology), Neuroblastoma, Neurotoxicity Syndromes (etiology), Neurotoxicity Syndromes (pathology), Neurotoxicity Syndromes (therapy), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Rats, Rotarod Performance Test (methods), Substantia Nigra (metabolism), Substantia Nigra (pathology), Superoxide Dismutase (metabolism), Superoxide Dismutase (therapeutic use), Tetrazolium Salts, Thiazoles, Transgenes (physiology), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , metabolism : Superoxide Dismutase, Tyrosine 3-Monooxygenase.
- chemical , therapeutic use : Superoxide Dismutase.
- chemical , toxicity : 1-Methyl-4-phenylpyridinium.
- etiology : Neurotoxicity Syndromes.
- metabolism : Substantia Nigra.
- methods : Cell Count, Genetic Therapy, Immunohistochemistry, Rotarod Performance Test.
- pathology : Neurotoxicity Syndromes, Parkinson Disease, Substantia Nigra.
- physiology : Genetic Vectors, Motor Activity, Transgenes.
- physiopathology : Parkinson Disease.
- therapy : Neurotoxicity Syndromes, Parkinson Disease.
- Animals, Cell Line, Tumor, Disease Models, Animal, Female, Gene Transfer Techniques, Humans, Neuroblastoma, Rats, Tetrazolium Salts, Thiazoles.
Abstract
Oxidative stress has been suggested to be an important mediator of dopaminergic cell death in Parkinson's disease (PD). We investigated the neuroprotective potential of Cu/Zn superoxide dismutase (SOD1) overexpression in the rat substantia nigra (SN) following adenovirus-mediated gene transfer. Human dopaminergic SK-N-SH cells were transduced with adenoviral vectors expressing either human SOD1 (Ad-SOD1) or beta-galactosidase (Ad-betagal) before exposure to 1 mM of the 1-methyl-4-phenylpyridinium ion (MPP+). A strong neuroprotective effect of SOD1 gene transfer was observed in the SK-N-SH cells exposed to MPP+ compared with controls. Adult rats were then given unilateral injections of either Ad-SOD1 or Ad-betagal into the striatum, and MPP+ was administered 8 days later at the same location. Strong transgene expression was detected in the SN dopaminergic neurons, a consequence of retrograde axonal transport of the adenoviral particles. The amphetamine-induced rotational behavior of the rats was markedly lower in Ad-SOD1-injected rats than in control animals. Also, behavioral recovery significantly correlated with the number of tyrosine hydrolase-expressing neurons in the SN of the treated rats. These results are consistent with oxidative stress contributing to the MPP+ -induced neurodegenerative process. They also indicate that SOD1 gene transfer into the nigrostriatal system may be a potential neuroprotective strategy for treating PD.
DOI: 10.1002/jnr.20696
PubMed: 16353238
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Horellou</name></author><author><name sortKey="Colin, Philippe" sort="Colin, Philippe" uniqKey="Colin P" first="Philippe" last="Colin">Philippe Colin</name></author><author><name sortKey="Millecamps, Stephanie" sort="Millecamps, Stephanie" uniqKey="Millecamps S" first="Stéphanie" last="Millecamps">Stéphanie Millecamps</name></author><author><name sortKey="Faucon Biguet, Nicole" sort="Faucon Biguet, Nicole" uniqKey="Faucon Biguet N" first="Nicole" last="Faucon-Biguet">Nicole Faucon-Biguet</name></author><author><name sortKey="Mallet, Jacques" sort="Mallet, Jacques" uniqKey="Mallet J" first="Jacques" last="Mallet">Jacques Mallet</name></author></analytic><series><title level="j">Journal of neuroscience research</title><idno type="ISSN">0360-4012</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenylpyridinium (toxicity)</term><term>Animals</term><term>Cell Count (methods)</term><term>Cell Line, Tumor</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Transfer Techniques</term><term>Genetic Therapy (methods)</term><term>Genetic Vectors (physiology)</term><term>Humans</term><term>Immunohistochemistry (methods)</term><term>Motor Activity (physiology)</term><term>Neuroblastoma</term><term>Neurotoxicity Syndromes (etiology)</term><term>Neurotoxicity Syndromes (pathology)</term><term>Neurotoxicity Syndromes (therapy)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Rats</term><term>Rotarod Performance Test (methods)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Superoxide Dismutase (metabolism)</term><term>Superoxide Dismutase (therapeutic use)</term><term>Tetrazolium Salts</term><term>Thiazoles</term><term>Transgenes (physiology)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Superoxide Dismutase</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>1-Methyl-4-phenylpyridinium</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Neurotoxicity Syndromes</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Cell Count</term><term>Genetic Therapy</term><term>Immunohistochemistry</term><term>Rotarod Performance Test</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurotoxicity Syndromes</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Genetic Vectors</term><term>Motor Activity</term><term>Transgenes</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Neurotoxicity Syndromes</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Transfer Techniques</term><term>Humans</term><term>Neuroblastoma</term><term>Rats</term><term>Tetrazolium Salts</term><term>Thiazoles</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative stress has been suggested to be an important mediator of dopaminergic cell death in Parkinson's disease (PD). We investigated the neuroprotective potential of Cu/Zn superoxide dismutase (SOD1) overexpression in the rat substantia nigra (SN) following adenovirus-mediated gene transfer. Human dopaminergic SK-N-SH cells were transduced with adenoviral vectors expressing either human SOD1 (Ad-SOD1) or beta-galactosidase (Ad-betagal) before exposure to 1 mM of the 1-methyl-4-phenylpyridinium ion (MPP+). A strong neuroprotective effect of SOD1 gene transfer was observed in the SK-N-SH cells exposed to MPP+ compared with controls. Adult rats were then given unilateral injections of either Ad-SOD1 or Ad-betagal into the striatum, and MPP+ was administered 8 days later at the same location. Strong transgene expression was detected in the SN dopaminergic neurons, a consequence of retrograde axonal transport of the adenoviral particles. The amphetamine-induced rotational behavior of the rats was markedly lower in Ad-SOD1-injected rats than in control animals. Also, behavioral recovery significantly correlated with the number of tyrosine hydrolase-expressing neurons in the SN of the treated rats. These results are consistent with oxidative stress contributing to the MPP+ -induced neurodegenerative process. They also indicate that SOD1 gene transfer into the nigrostriatal system may be a potential neuroprotective strategy for treating PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16353238</PMID><DateCreated><Year>2006</Year><Month>01</Month><Day>25</Day></DateCreated><DateCompleted><Year>2006</Year><Month>05</Month><Day>25</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0360-4012</ISSN><JournalIssue CitedMedium="Print"><Volume>83</Volume><Issue>2</Issue><PubDate><Year>2006</Year><Month>Feb</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of neuroscience research</Title><ISOAbbreviation>J. Neurosci. Res.</ISOAbbreviation></Journal><ArticleTitle>1-methyl-4-phenylpyridinium neurotoxicity is attenuated by adenoviral gene transfer of human Cu/Zn superoxide dismutase.</ArticleTitle><Pagination><MedlinePgn>233-42</MedlinePgn></Pagination><Abstract><AbstractText>Oxidative stress has been suggested to be an important mediator of dopaminergic cell death in Parkinson's disease (PD). We investigated the neuroprotective potential of Cu/Zn superoxide dismutase (SOD1) overexpression in the rat substantia nigra (SN) following adenovirus-mediated gene transfer. Human dopaminergic SK-N-SH cells were transduced with adenoviral vectors expressing either human SOD1 (Ad-SOD1) or beta-galactosidase (Ad-betagal) before exposure to 1 mM of the 1-methyl-4-phenylpyridinium ion (MPP+). A strong neuroprotective effect of SOD1 gene transfer was observed in the SK-N-SH cells exposed to MPP+ compared with controls. Adult rats were then given unilateral injections of either Ad-SOD1 or Ad-betagal into the striatum, and MPP+ was administered 8 days later at the same location. Strong transgene expression was detected in the SN dopaminergic neurons, a consequence of retrograde axonal transport of the adenoviral particles. The amphetamine-induced rotational behavior of the rats was markedly lower in Ad-SOD1-injected rats than in control animals. Also, behavioral recovery significantly correlated with the number of tyrosine hydrolase-expressing neurons in the SN of the treated rats. These results are consistent with oxidative stress contributing to the MPP+ -induced neurodegenerative process. They also indicate that SOD1 gene transfer into the nigrostriatal system may be a potential neuroprotective strategy for treating PD.</AbstractText><CopyrightInformation>Copyright 2005 Wiley-Liss, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Barkats</LastName><ForeName>Martine</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs (LGN), CNRS UMR 7091, Paris, France. barkats@genethon.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Horellou</LastName><ForeName>Philippe</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Colin</LastName><ForeName>Philippe</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Millecamps</LastName><ForeName>Stéphanie</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Faucon-Biguet</LastName><ForeName>Nicole</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Mallet</LastName><ForeName>Jacques</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurosci Res</MedlineTA><NlmUniqueID>7600111</NlmUniqueID><ISSNLinking>0360-4012</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013778">Tetrazolium Salts</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013844">Thiazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 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