Corpus
PascalFrancis
Racine
Corpus
Checkpoint
PascalFrancis
Racine
PascalFrancis
Exploration
Accueil
Racine
Racine

La maladie de Parkinson en France (serveur d'exploration)

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease

Identifieur interne : 000D77 ( PascalFrancis/Corpus ); précédent : 000D76; suivant : 000D78

Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease

Auteurs : N. A. Do Thi ; P. Saillour ; L. Ferrero ; I. F. Dedieu ; J. Mallet ; T. Paunio

Source :

RBID : Pascal:04-0453384

Descripteurs français

English descriptors

Abstract

A new adenoviral vector (Ad-GFAP-GDNF) (Ad= adenovirus, GFAP= glial fibrillary acidic protein, GDNF = glial cell line-derived neurotrophic factor) was constructed in which (i) the E1,E3/E4 regions of Ad5 were deleted and (ii) the GDNF transgene is driven by the GFAP promoter. We verified, in vitro, that the recombinant GDNF was expressed in primary cultures of astrocytes. In vivo, the Ad-GFAP-GDNF was injected into the striatum of rats 1 week before provoking striatal 6-OHDA lesion. After 1 month, the striatal GDNF levels were 37pg/μg total protein. This quantity was at least 120-fold higher than in nontransduced striatum or after injection of the empty adenoviral vector. At 3 months after viral injection, GDNF expression decreased, whereas the viral DNA remained unchanged. Furthermore, around 70% of the dopaminergic (DA) neurons were protected from degeneration up to 3 months as compared to about 45% in the control groups. In addition, the amphetamine-induced rotational behavior was decreased. The results obtained in this study on DA neuron protection and rotational behavior are similar to those previously reported using vectors with viral promoters. In addition to these results, we established that a high level of GDNF was present in the striatum and that the period of GDNF expression was prolonged after injection of our adenoviral vector.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 0969-7128
A03   1    @0 Gene ther. : (Basingstoke)
A05       @2 11
A06       @2 9
A08 01  1  ENG  @1 Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease
A11 01  1    @1 DO THI (N. A.)
A11 02  1    @1 SAILLOUR (P.)
A11 03  1    @1 FERRERO (L.)
A11 04  1    @1 DEDIEU (I. F.)
A11 05  1    @1 MALLET (J.)
A11 06  1    @1 PAUNIO (T.)
A14 01      @1 Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere @2 Paris @3 FRA @Z 1 aut. @Z 2 aut. @Z 5 aut. @Z 6 aut.
A14 02      @1 Gencell SAS @2 Vitry sur Seine @3 FRA @Z 3 aut. @Z 4 aut.
A14 03      @1 Department of Molecular Medicine, Biomedicum @2 Helsinki @3 FIN @Z 6 aut.
A20       @1 746-756
A21       @1 2004
A23 01      @0 ENG
A43 01      @1 INIST @2 26274 @5 354000110234630020
A44       @0 0000 @1 © 2004 INIST-CNRS. All rights reserved.
A45       @0 44 ref.
A47 01  1    @0 04-0453384
A60       @1 P
A61       @0 A
A64 01  1    @0 Gene therapy : (Basingstoke)
A66 01      @0 GBR
C01 01    ENG  @0 A new adenoviral vector (Ad-GFAP-GDNF) (Ad= adenovirus, GFAP= glial fibrillary acidic protein, GDNF = glial cell line-derived neurotrophic factor) was constructed in which (i) the E1,E3/E4 regions of Ad5 were deleted and (ii) the GDNF transgene is driven by the GFAP promoter. We verified, in vitro, that the recombinant GDNF was expressed in primary cultures of astrocytes. In vivo, the Ad-GFAP-GDNF was injected into the striatum of rats 1 week before provoking striatal 6-OHDA lesion. After 1 month, the striatal GDNF levels were 37pg/μg total protein. This quantity was at least 120-fold higher than in nontransduced striatum or after injection of the empty adenoviral vector. At 3 months after viral injection, GDNF expression decreased, whereas the viral DNA remained unchanged. Furthermore, around 70% of the dopaminergic (DA) neurons were protected from degeneration up to 3 months as compared to about 45% in the control groups. In addition, the amphetamine-induced rotational behavior was decreased. The results obtained in this study on DA neuron protection and rotational behavior are similar to those previously reported using vectors with viral promoters. In addition to these results, we established that a high level of GDNF was present in the striatum and that the period of GDNF expression was prolonged after injection of our adenoviral vector.
C02 01  X    @0 002A31D01D
C02 02  X    @0 002B27D03
C02 03  X    @0 002B17G
C02 04  X    @0 215
C03 01  X  FRE  @0 Adenoviridae @2 NW @5 01
C03 01  X  ENG  @0 Adenoviridae @2 NW @5 01
C03 01  X  SPA  @0 Adenoviridae @2 NW @5 01
C03 02  X  FRE  @0 Thérapie génique @5 02
C03 02  X  ENG  @0 Gene therapy @5 02
C03 02  X  SPA  @0 Terapia génica @5 02
C03 03  X  FRE  @0 Vecteur @5 03
C03 03  X  ENG  @0 Vector @5 03
C03 03  X  SPA  @0 Vector @5 03
C03 04  X  FRE  @0 Neurone dopaminergique @5 04
C03 04  X  ENG  @0 Dopaminergic neuron @5 04
C03 04  X  SPA  @0 Neurona dopaminérgica @5 04
C03 05  X  FRE  @0 Dégénérescence @5 05
C03 05  X  ENG  @0 Degeneration @5 05
C03 05  X  SPA  @0 Degeneración @5 05
C03 06  X  FRE  @0 Rat @5 06
C03 06  X  ENG  @0 Rat @5 06
C03 06  X  SPA  @0 Rata @5 06
C03 07  X  FRE  @0 Modèle animal @5 07
C03 07  X  ENG  @0 Animal model @5 07
C03 07  X  SPA  @0 Modelo animal @5 07
C03 08  X  FRE  @0 Protéine gliofibrillaire @5 08
C03 08  X  ENG  @0 Glial fibrillary acidic protein @5 08
C03 08  X  SPA  @0 Proteína gliofibrilar @5 08
C03 09  X  FRE  @0 Facteur GDNF @5 09
C03 09  X  ENG  @0 Glial cell line derived neurotrophic factor @5 09
C03 09  X  SPA  @0 Factor GDNF @5 09
C03 10  X  FRE  @0 Parkinson maladie @5 14
C03 10  X  ENG  @0 Parkinson disease @5 14
C03 10  X  SPA  @0 Parkinson enfermedad @5 14
C07 01  X  FRE  @0 Virus @2 NW
C07 01  X  ENG  @0 Virus @2 NW
C07 01  X  SPA  @0 Virus @2 NW
C07 02  X  FRE  @0 Rodentia @2 NS
C07 02  X  ENG  @0 Rodentia @2 NS
C07 02  X  SPA  @0 Rodentia @2 NS
C07 03  X  FRE  @0 Mammalia @2 NS
C07 03  X  ENG  @0 Mammalia @2 NS
C07 03  X  SPA  @0 Mammalia @2 NS
C07 04  X  FRE  @0 Vertebrata @2 NS
C07 04  X  ENG  @0 Vertebrata @2 NS
C07 04  X  SPA  @0 Vertebrata @2 NS
C07 05  X  FRE  @0 Encéphale pathologie @5 19
C07 05  X  ENG  @0 Cerebral disorder @5 19
C07 05  X  SPA  @0 Encéfalo patología @5 19
C07 06  X  FRE  @0 Extrapyramidal syndrome @5 20
C07 06  X  ENG  @0 Extrapyramidal syndrome @5 20
C07 06  X  SPA  @0 Extrapiramidal síndrome @5 20
C07 07  X  FRE  @0 Maladie dégénérative @5 21
C07 07  X  ENG  @0 Degenerative disease @5 21
C07 07  X  SPA  @0 Enfermedad degenerativa @5 21
C07 08  X  FRE  @0 Système nerveux central pathologie @5 22
C07 08  X  ENG  @0 Central nervous system disease @5 22
C07 08  X  SPA  @0 Sistema nervosio central patología @5 22
C07 09  X  FRE  @0 Système nerveux pathologie @5 23
C07 09  X  ENG  @0 Nervous system diseases @5 23
C07 09  X  SPA  @0 Sistema nervioso patología @5 23
N21       @1 257
N44 01      @1 PSI
N82       @1 PSI

Format Inist (serveur)

NO : PASCAL 04-0453384 INIST
ET : Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease
AU : DO THI (N. A.); SAILLOUR (P.); FERRERO (L.); DEDIEU (I. F.); MALLET (J.); PAUNIO (T.)
AF : Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere/Paris/France (1 aut., 2 aut., 5 aut., 6 aut.); Gencell SAS/Vitry sur Seine/France (3 aut., 4 aut.); Department of Molecular Medicine, Biomedicum/Helsinki/Finlande (6 aut.)
DT : Publication en série; Niveau analytique
SO : Gene therapy : (Basingstoke); ISSN 0969-7128; Royaume-Uni; Da. 2004; Vol. 11; No. 9; Pp. 746-756; Bibl. 44 ref.
LA : Anglais
EA : A new adenoviral vector (Ad-GFAP-GDNF) (Ad= adenovirus, GFAP= glial fibrillary acidic protein, GDNF = glial cell line-derived neurotrophic factor) was constructed in which (i) the E1,E3/E4 regions of Ad5 were deleted and (ii) the GDNF transgene is driven by the GFAP promoter. We verified, in vitro, that the recombinant GDNF was expressed in primary cultures of astrocytes. In vivo, the Ad-GFAP-GDNF was injected into the striatum of rats 1 week before provoking striatal 6-OHDA lesion. After 1 month, the striatal GDNF levels were 37pg/μg total protein. This quantity was at least 120-fold higher than in nontransduced striatum or after injection of the empty adenoviral vector. At 3 months after viral injection, GDNF expression decreased, whereas the viral DNA remained unchanged. Furthermore, around 70% of the dopaminergic (DA) neurons were protected from degeneration up to 3 months as compared to about 45% in the control groups. In addition, the amphetamine-induced rotational behavior was decreased. The results obtained in this study on DA neuron protection and rotational behavior are similar to those previously reported using vectors with viral promoters. In addition to these results, we established that a high level of GDNF was present in the striatum and that the period of GDNF expression was prolonged after injection of our adenoviral vector.
CC : 002A31D01D; 002B27D03; 002B17G; 215
FD : Adenoviridae; Thérapie génique; Vecteur; Neurone dopaminergique; Dégénérescence; Rat; Modèle animal; Protéine gliofibrillaire; Facteur GDNF; Parkinson maladie
FG : Virus; Rodentia; Mammalia; Vertebrata; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie
ED : Adenoviridae; Gene therapy; Vector; Dopaminergic neuron; Degeneration; Rat; Animal model; Glial fibrillary acidic protein; Glial cell line derived neurotrophic factor; Parkinson disease
EG : Virus; Rodentia; Mammalia; Vertebrata; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases
SD : Adenoviridae; Terapia génica; Vector; Neurona dopaminérgica; Degeneración; Rata; Modelo animal; Proteína gliofibrilar; Factor GDNF; Parkinson enfermedad
LO : INIST-26274.354000110234630020
ID : 04-0453384

Links to Exploration step

Pascal:04-0453384

Le document en format XML

<record>
<TEI>
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en" level="a">Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease</title>
<author>
<name sortKey="Do Thi, N A" sort="Do Thi, N A" uniqKey="Do Thi N" first="N. A." last="Do Thi">N. A. Do Thi</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Saillour, P" sort="Saillour, P" uniqKey="Saillour P" first="P." last="Saillour">P. Saillour</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Ferrero, L" sort="Ferrero, L" uniqKey="Ferrero L" first="L." last="Ferrero">L. Ferrero</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Gencell SAS</s1>
<s2>Vitry sur Seine</s2>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Dedieu, I F" sort="Dedieu, I F" uniqKey="Dedieu I" first="I. F." last="Dedieu">I. F. Dedieu</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Gencell SAS</s1>
<s2>Vitry sur Seine</s2>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Mallet, J" sort="Mallet, J" uniqKey="Mallet J" first="J." last="Mallet">J. Mallet</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Paunio, T" sort="Paunio, T" uniqKey="Paunio T" first="T." last="Paunio">T. Paunio</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation>
<inist:fA14 i1="03">
<s1>Department of Molecular Medicine, Biomedicum</s1>
<s2>Helsinki</s2>
<s3>FIN</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">INIST</idno>
<idno type="inist">04-0453384</idno>
<date when="2004">2004</date>
<idno type="stanalyst">PASCAL 04-0453384 INIST</idno>
<idno type="RBID">Pascal:04-0453384</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000D77</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en" level="a">Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease</title>
<author>
<name sortKey="Do Thi, N A" sort="Do Thi, N A" uniqKey="Do Thi N" first="N. A." last="Do Thi">N. A. Do Thi</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Saillour, P" sort="Saillour, P" uniqKey="Saillour P" first="P." last="Saillour">P. Saillour</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Ferrero, L" sort="Ferrero, L" uniqKey="Ferrero L" first="L." last="Ferrero">L. Ferrero</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Gencell SAS</s1>
<s2>Vitry sur Seine</s2>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Dedieu, I F" sort="Dedieu, I F" uniqKey="Dedieu I" first="I. F." last="Dedieu">I. F. Dedieu</name>
<affiliation>
<inist:fA14 i1="02">
<s1>Gencell SAS</s1>
<s2>Vitry sur Seine</s2>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Mallet, J" sort="Mallet, J" uniqKey="Mallet J" first="J." last="Mallet">J. Mallet</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Paunio, T" sort="Paunio, T" uniqKey="Paunio T" first="T." last="Paunio">T. Paunio</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation>
<inist:fA14 i1="03">
<s1>Department of Molecular Medicine, Biomedicum</s1>
<s2>Helsinki</s2>
<s3>FIN</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series>
<title level="j" type="main">Gene therapy : (Basingstoke)</title>
<title level="j" type="abbreviated">Gene ther. : (Basingstoke)</title>
<idno type="ISSN">0969-7128</idno>
<imprint>
<date when="2004">2004</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt>
<title level="j" type="main">Gene therapy : (Basingstoke)</title>
<title level="j" type="abbreviated">Gene ther. : (Basingstoke)</title>
<idno type="ISSN">0969-7128</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Adenoviridae</term>
<term>Animal model</term>
<term>Degeneration</term>
<term>Dopaminergic neuron</term>
<term>Gene therapy</term>
<term>Glial cell line derived neurotrophic factor</term>
<term>Glial fibrillary acidic protein</term>
<term>Parkinson disease</term>
<term>Rat</term>
<term>Vector</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Adenoviridae</term>
<term>Thérapie génique</term>
<term>Vecteur</term>
<term>Neurone dopaminergique</term>
<term>Dégénérescence</term>
<term>Rat</term>
<term>Modèle animal</term>
<term>Protéine gliofibrillaire</term>
<term>Facteur GDNF</term>
<term>Parkinson maladie</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">A new adenoviral vector (Ad-GFAP-GDNF) (Ad= adenovirus, GFAP= glial fibrillary acidic protein, GDNF = glial cell line-derived neurotrophic factor) was constructed in which (i) the E1,E3/E4 regions of Ad5 were deleted and (ii) the GDNF transgene is driven by the GFAP promoter. We verified, in vitro, that the recombinant GDNF was expressed in primary cultures of astrocytes. In vivo, the Ad-GFAP-GDNF was injected into the striatum of rats 1 week before provoking striatal 6-OHDA lesion. After 1 month, the striatal GDNF levels were 37pg/μg total protein. This quantity was at least 120-fold higher than in nontransduced striatum or after injection of the empty adenoviral vector. At 3 months after viral injection, GDNF expression decreased, whereas the viral DNA remained unchanged. Furthermore, around 70% of the dopaminergic (DA) neurons were protected from degeneration up to 3 months as compared to about 45% in the control groups. In addition, the amphetamine-induced rotational behavior was decreased. The results obtained in this study on DA neuron protection and rotational behavior are similar to those previously reported using vectors with viral promoters. In addition to these results, we established that a high level of GDNF was present in the striatum and that the period of GDNF expression was prolonged after injection of our adenoviral vector.</div>
</front>
</TEI>
<inist>
<standard h6="B">
<pA>
<fA01 i1="01" i2="1">
<s0>0969-7128</s0>
</fA01>
<fA03 i2="1">
<s0>Gene ther. : (Basingstoke)</s0>
</fA03>
<fA05>
<s2>11</s2>
</fA05>
<fA06>
<s2>9</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG">
<s1>Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease</s1>
</fA08>
<fA11 i1="01" i2="1">
<s1>DO THI (N. A.)</s1>
</fA11>
<fA11 i1="02" i2="1">
<s1>SAILLOUR (P.)</s1>
</fA11>
<fA11 i1="03" i2="1">
<s1>FERRERO (L.)</s1>
</fA11>
<fA11 i1="04" i2="1">
<s1>DEDIEU (I. F.)</s1>
</fA11>
<fA11 i1="05" i2="1">
<s1>MALLET (J.)</s1>
</fA11>
<fA11 i1="06" i2="1">
<s1>PAUNIO (T.)</s1>
</fA11>
<fA14 i1="01">
<s1>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Gencell SAS</s1>
<s2>Vitry sur Seine</s2>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>Department of Molecular Medicine, Biomedicum</s1>
<s2>Helsinki</s2>
<s3>FIN</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20>
<s1>746-756</s1>
</fA20>
<fA21>
<s1>2004</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>26274</s2>
<s5>354000110234630020</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2004 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>44 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>04-0453384</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Gene therapy : (Basingstoke)</s0>
</fA64>
<fA66 i1="01">
<s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>A new adenoviral vector (Ad-GFAP-GDNF) (Ad= adenovirus, GFAP= glial fibrillary acidic protein, GDNF = glial cell line-derived neurotrophic factor) was constructed in which (i) the E1,E3/E4 regions of Ad5 were deleted and (ii) the GDNF transgene is driven by the GFAP promoter. We verified, in vitro, that the recombinant GDNF was expressed in primary cultures of astrocytes. In vivo, the Ad-GFAP-GDNF was injected into the striatum of rats 1 week before provoking striatal 6-OHDA lesion. After 1 month, the striatal GDNF levels were 37pg/μg total protein. This quantity was at least 120-fold higher than in nontransduced striatum or after injection of the empty adenoviral vector. At 3 months after viral injection, GDNF expression decreased, whereas the viral DNA remained unchanged. Furthermore, around 70% of the dopaminergic (DA) neurons were protected from degeneration up to 3 months as compared to about 45% in the control groups. In addition, the amphetamine-induced rotational behavior was decreased. The results obtained in this study on DA neuron protection and rotational behavior are similar to those previously reported using vectors with viral promoters. In addition to these results, we established that a high level of GDNF was present in the striatum and that the period of GDNF expression was prolonged after injection of our adenoviral vector.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002A31D01D</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B27D03</s0>
</fC02>
<fC02 i1="03" i2="X">
<s0>002B17G</s0>
</fC02>
<fC02 i1="04" i2="X">
<s0>215</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Adenoviridae</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Adenoviridae</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Adenoviridae</s0>
<s2>NW</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Thérapie génique</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Gene therapy</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Terapia génica</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Vecteur</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Vector</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Vector</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Neurone dopaminergique</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Dopaminergic neuron</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Neurona dopaminérgica</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Dégénérescence</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Degeneration</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Degeneración</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Rat</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Rat</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Rata</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Modèle animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Animal model</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Modelo animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Protéine gliofibrillaire</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Glial fibrillary acidic protein</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Proteína gliofibrilar</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Facteur GDNF</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Glial cell line derived neurotrophic factor</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Factor GDNF</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>19</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>19</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>19</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>20</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>20</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>20</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>21</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>21</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>21</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>22</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>22</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>23</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>23</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>23</s5>
</fC07>
<fN21>
<s1>257</s1>
</fN21>
<fN44 i1="01">
<s1>PSI</s1>
</fN44>
<fN82>
<s1>PSI</s1>
</fN82>
</pA>
</standard>
<server>
<NO>PASCAL 04-0453384 INIST</NO>
<ET>Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease</ET>
<AU>DO THI (N. A.); SAILLOUR (P.); FERRERO (L.); DEDIEU (I. F.); MALLET (J.); PAUNIO (T.)</AU>
<AF>Laboratoire de Genetique Moleculaire de la Neurotransmission et des Processus Neurodegeneratifs, CNRS, Bat. CERVI, Hopital Pitie-Salpetriere/Paris/France (1 aut., 2 aut., 5 aut., 6 aut.); Gencell SAS/Vitry sur Seine/France (3 aut., 4 aut.); Department of Molecular Medicine, Biomedicum/Helsinki/Finlande (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Gene therapy : (Basingstoke); ISSN 0969-7128; Royaume-Uni; Da. 2004; Vol. 11; No. 9; Pp. 746-756; Bibl. 44 ref.</SO>
<LA>Anglais</LA>
<EA>A new adenoviral vector (Ad-GFAP-GDNF) (Ad= adenovirus, GFAP= glial fibrillary acidic protein, GDNF = glial cell line-derived neurotrophic factor) was constructed in which (i) the E1,E3/E4 regions of Ad5 were deleted and (ii) the GDNF transgene is driven by the GFAP promoter. We verified, in vitro, that the recombinant GDNF was expressed in primary cultures of astrocytes. In vivo, the Ad-GFAP-GDNF was injected into the striatum of rats 1 week before provoking striatal 6-OHDA lesion. After 1 month, the striatal GDNF levels were 37pg/μg total protein. This quantity was at least 120-fold higher than in nontransduced striatum or after injection of the empty adenoviral vector. At 3 months after viral injection, GDNF expression decreased, whereas the viral DNA remained unchanged. Furthermore, around 70% of the dopaminergic (DA) neurons were protected from degeneration up to 3 months as compared to about 45% in the control groups. In addition, the amphetamine-induced rotational behavior was decreased. The results obtained in this study on DA neuron protection and rotational behavior are similar to those previously reported using vectors with viral promoters. In addition to these results, we established that a high level of GDNF was present in the striatum and that the period of GDNF expression was prolonged after injection of our adenoviral vector.</EA>
<CC>002A31D01D; 002B27D03; 002B17G; 215</CC>
<FD>Adenoviridae; Thérapie génique; Vecteur; Neurone dopaminergique; Dégénérescence; Rat; Modèle animal; Protéine gliofibrillaire; Facteur GDNF; Parkinson maladie</FD>
<FG>Virus; Rodentia; Mammalia; Vertebrata; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie</FG>
<ED>Adenoviridae; Gene therapy; Vector; Dopaminergic neuron; Degeneration; Rat; Animal model; Glial fibrillary acidic protein; Glial cell line derived neurotrophic factor; Parkinson disease</ED>
<EG>Virus; Rodentia; Mammalia; Vertebrata; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases</EG>
<SD>Adenoviridae; Terapia génica; Vector; Neurona dopaminérgica; Degeneración; Rata; Modelo animal; Proteína gliofibrilar; Factor GDNF; Parkinson enfermedad</SD>
<LO>INIST-26274.354000110234630020</LO>
<ID>04-0453384</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PascalFrancis/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000D77 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000D77 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Sante
   |area=    ParkinsonFranceV1
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:04-0453384
   |texte=   Delivery of GDNF by an E1,E3/E4 deleted adenoviral vector and driven by a GFAP promoter prevents dopaminergic neuron degeneration in a rat model of Parkinson's disease
}}
Wicri

This area was generated with Dilib version V0.6.29.
Data generation: Wed May 17 19:46:39 2017. Site generation: Mon Mar 4 15:48:15 2024