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 : 000657 ( PascalFrancis/Curation ); précédent : 000656; suivant : 000658Delivery 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 [France] ; P. Saillour [France] ; L. Ferrero [France] ; I. F. Dedieu [France] ; J. Mallet [France] ; T. Paunio [France, Finlande]Source :
- Gene therapy : (Basingstoke) [ 0969-7128 ] ; 2004.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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<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>
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<s5>19</s5>
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<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>
</inist>
</record>
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