Does neuronal expression of GDNF effectively protect dopaminergic neurons in a rat model of Parkinson's disease?
Identifieur interne : 002881 ( Main/Merge ); précédent : 002880; suivant : 002882Does neuronal expression of GDNF effectively protect dopaminergic neurons in a rat model of Parkinson's disease?
Auteurs : N A Do Thi [France] ; P. Saillour ; L. Ferrero ; T. Paunio ; J. MalletSource :
- Gene therapy [ 0969-7128 ] ; 2007.
English descriptors
- KwdEn :
- Adenoviridae (genetics), Animals, Astrocytes (metabolism), Cells, Cultured, Corpus Striatum (metabolism), Dopamine (metabolism), Female, Gene Expression, Genetic Therapy (methods), Genetic Vectors (administration & dosage), Glial Cell Line-Derived Neurotrophic Factor (genetics), Glial Cell Line-Derived Neurotrophic Factor (metabolism), Mesencephalon (metabolism), Neurons (metabolism), Parkinson Disease (metabolism), Phosphopyruvate Hydratase (genetics), Promoter Regions, Genetic, Rats, Rats, Sprague-Dawley, Substantia Nigra (metabolism), Transduction, Genetic (methods), Transgenes.
- MESH :
- chemical , genetics : Glial Cell Line-Derived Neurotrophic Factor, Phosphopyruvate Hydratase.
- chemical , metabolism : Dopamine, Glial Cell Line-Derived Neurotrophic Factor.
- administration & dosage : Genetic Vectors.
- genetics : Adenoviridae.
- metabolism : Astrocytes, Corpus Striatum, Mesencephalon, Neurons, Parkinson Disease, Substantia Nigra.
- methods : Genetic Therapy, Transduction, Genetic.
- Animals, Cells, Cultured, Female, Gene Expression, Promoter Regions, Genetic, Rats, Rats, Sprague-Dawley, Transgenes.
Abstract
The transfer of the Glial cell line-derived neurotrophic factor (GDNF) gene to the central nervous system by a recombinant adenoviral vector (Ad) was studied. We constructed the adenovirus vector Ad-NSE-GDNF from which the E1, E3/E4 regions of Ad5 have been deleted and in which the GDNF gene was under the control of a neuron-specific enolase (NSE) promoter. The vector was injected into the striatum of a rat model of Parkinson's disease. We found that (i) the NSE promoter can restrict transgene expression in neurons; (ii) Ad-NSE-GDNF significantly protected dopaminergic (DA) neurons in the substantia nigra (SN) but did not reverse the impairments of amphetamine-induced rotational behavior in lesioned rats.
Url:
DOI: 10.1038/sj.gt.3302844
PubMed: 17093508
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pubmed:17093508Le document en format XML
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term>
<term>Glial Cell Line-Derived Neurotrophic Factor</term>
</keywords>
<keywords scheme="MESH" qualifier="administration & dosage" xml:lang="en"><term>Genetic Vectors</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term>
<term>Corpus Striatum</term>
<term>Mesencephalon</term>
<term>Neurons</term>
<term>Parkinson Disease</term>
<term>Substantia Nigra</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Genetic Therapy</term>
<term>Transduction, Genetic</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cells, Cultured</term>
<term>Female</term>
<term>Gene Expression</term>
<term>Promoter Regions, Genetic</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Transgenes</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The transfer of the Glial cell line-derived neurotrophic factor (GDNF) gene to the central nervous system by a recombinant adenoviral vector (Ad) was studied. We constructed the adenovirus vector Ad-NSE-GDNF from which the E1, E3/E4 regions of Ad5 have been deleted and in which the GDNF gene was under the control of a neuron-specific enolase (NSE) promoter. The vector was injected into the striatum of a rat model of Parkinson's disease. We found that (i) the NSE promoter can restrict transgene expression in neurons; (ii) Ad-NSE-GDNF significantly protected dopaminergic (DA) neurons in the substantia nigra (SN) but did not reverse the impairments of amphetamine-induced rotational behavior in lesioned rats.</div>
</front>
</TEI>
</PubMed>
</double>
</record>
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