MovDisordV3, PascalFrancis, Curation, bibRecord, 000300

Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice

Identifieur interne : 000300 ( PascalFrancis/Curation ); précédent : 000299; suivant : 000301

Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice

Auteurs : Hélène Turmel [France] ; Andreas Hartmann [France] ; Karine Parain [France] ; Aicha Doubou [France] ; Anu Srinivasan [États-Unis] ; Yves Agid [France] ; Etienne C. Hirsch [France]

Source :

Movement disorders [ 0885-3185 ] ; 2001.

RBID : Pascal:01-0333747

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Activité enzymatique, Apoptose, Modèle animal, Pathogénie, Souris, Animal, Caspase 3.

English descriptors

KwdEn :
- Animal, Animal model, Apoptosis, Enzymatic activity, Mouse, Parkinson disease, Pathogenesis.

Abstract

In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP⁺) may be mediated by caspase-3. To establish whether caspase-3 activation may indeed play a role in an in vivo model of PD, we studied caspase-3 activation in C57B1/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days I and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase-3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo.

A01	`01`	`1`		`@0 0885-3185`
A03		`1`		`@0 Mov. disord.`
A05				`@2 16`
A06				`@2 2`
A08	`01`	`1`	`ENG`	`@1 Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice`
A11	`01`	`1`		`@1 TURMEL (Hélène)`
A11	`02`	`1`		`@1 HARTMANN (Andreas)`
A11	`03`	`1`		`@1 PARAIN (Karine)`
A11	`04`	`1`		`@1 DOUBOU (Aicha)`
A11	`05`	`1`		`@1 SRINIVASAN (Anu)`
A11	`06`	`1`		`@1 AGID (Yves)`
A11	`07`	`1`		`@1 HIRSCH (Etienne C.)`
A14	`01`			`@1 INSERM U 289, Hópital de la Salpétrière @2 Paris @3 FRA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 6 aut. @Z 7 aut.`
A14	`02`			`@1 IDUN Pharmaceuticals Inc. @2 La Jolla, California @3 USA @Z 5 aut.`
A20				`@1 185-189`
A21				`@1 2001`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 20953 @5 354000096545190020`
A44				`@0 0000 @1 © 2001 INIST-CNRS. All rights reserved.`
A45				`@0 17 ref.`
A47	`01`	`1`		`@0 01-0333747`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Movement disorders`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP⁺) may be mediated by caspase-3. To establish whether caspase-3 activation may indeed play a role in an in vivo model of PD, we studied caspase-3 activation in C57B1/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days I and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase-3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo.
C02	`01`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Parkinson maladie @5 01`
C03	`01`	`X`	`ENG`	`@0 Parkinson disease @5 01`
C03	`01`	`X`	`SPA`	`@0 Parkinson enfermedad @5 01`
C03	`02`	`X`	`FRE`	`@0 Activité enzymatique @5 07`
C03	`02`	`X`	`ENG`	`@0 Enzymatic activity @5 07`
C03	`02`	`X`	`SPA`	`@0 Actividad enzimática @5 07`
C03	`03`	`X`	`FRE`	`@0 Apoptose @5 10`
C03	`03`	`X`	`ENG`	`@0 Apoptosis @5 10`
C03	`03`	`X`	`SPA`	`@0 Apoptosis @5 10`
C03	`04`	`X`	`FRE`	`@0 Modèle animal @5 17`
C03	`04`	`X`	`ENG`	`@0 Animal model @5 17`
C03	`04`	`X`	`SPA`	`@0 Modelo animal @5 17`
C03	`05`	`X`	`FRE`	`@0 Pathogénie @5 18`
C03	`05`	`X`	`ENG`	`@0 Pathogenesis @5 18`
C03	`05`	`X`	`SPA`	`@0 Patogenia @5 18`
C03	`06`	`X`	`FRE`	`@0 Souris @5 20`
C03	`06`	`X`	`ENG`	`@0 Mouse @5 20`
C03	`06`	`X`	`SPA`	`@0 Ratón @5 20`
C03	`07`	`X`	`FRE`	`@0 Animal @5 21`
C03	`07`	`X`	`ENG`	`@0 Animal @5 21`
C03	`07`	`X`	`SPA`	`@0 Animal @5 21`
C03	`08`	`X`	`FRE`	`@0 Caspase 3 @2 FE @4 INC @5 86`
C07	`01`	`X`	`FRE`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`ENG`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`SPA`	`@0 Rodentia @2 NS`
C07	`02`	`X`	`FRE`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`ENG`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`03`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`SPA`	`@0 Vertebrata @2 NS`
C07	`04`	`X`	`FRE`	`@0 Système nerveux pathologie @5 37`
C07	`04`	`X`	`ENG`	`@0 Nervous system diseases @5 37`
C07	`04`	`X`	`SPA`	`@0 Sistema nervioso patología @5 37`
C07	`05`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 38`
C07	`05`	`X`	`ENG`	`@0 Central nervous system disease @5 38`
C07	`05`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 38`
C07	`06`	`X`	`FRE`	`@0 Encéphale pathologie @5 39`
C07	`06`	`X`	`ENG`	`@0 Cerebral disorder @5 39`
C07	`06`	`X`	`SPA`	`@0 Encéfalo patología @5 39`
C07	`07`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 40`
C07	`07`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 40`
C07	`07`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 40`
C07	`08`	`X`	`FRE`	`@0 Maladie dégénérative @5 41`
C07	`08`	`X`	`ENG`	`@0 Degenerative disease @5 41`
C07	`08`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 41`
C07	`09`	`X`	`FRE`	`@0 Cysteine endopeptidases @2 FE @5 45`
C07	`09`	`X`	`ENG`	`@0 Cysteine endopeptidases @2 FE @5 45`
C07	`09`	`X`	`SPA`	`@0 Cysteine endopeptidases @2 FE @5 45`
C07	`10`	`X`	`FRE`	`@0 Peptidases @2 FE`
C07	`10`	`X`	`ENG`	`@0 Peptidases @2 FE`
C07	`10`	`X`	`SPA`	`@0 Peptidases @2 FE`
C07	`11`	`X`	`FRE`	`@0 Hydrolases @2 FE`
C07	`11`	`X`	`ENG`	`@0 Hydrolases @2 FE`
C07	`11`	`X`	`SPA`	`@0 Hydrolases @2 FE`
C07	`12`	`X`	`FRE`	`@0 Enzyme`
C07	`12`	`X`	`ENG`	`@0 Enzyme`
C07	`12`	`X`	`SPA`	`@0 Enzima`
N21				`@1 232`

Links toward previous steps (curation, corpus...)

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Pascal:01-0333747

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice</title>
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<author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name>
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<series><title level="j" type="main">Movement disorders</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term>
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<front><div type="abstract" xml:lang="en">In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>
) may be mediated by caspase-3. To establish whether caspase-3 activation may indeed play a role in an in vivo model of PD, we studied caspase-3 activation in C57B1/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days I and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase-3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo.</div>
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<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>
) may be mediated by caspase-3. To establish whether caspase-3 activation may indeed play a role in an in vivo model of PD, we studied caspase-3 activation in C57B1/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days I and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase-3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Activité enzymatique</s0>
<s5>07</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Enzymatic activity</s0>
<s5>07</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Actividad enzimática</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Apoptose</s0>
<s5>10</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Apoptosis</s0>
<s5>10</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Apoptosis</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Modèle animal</s0>
<s5>17</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Animal model</s0>
<s5>17</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Modelo animal</s0>
<s5>17</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Pathogénie</s0>
<s5>18</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Pathogenesis</s0>
<s5>18</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Patogenia</s0>
<s5>18</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Souris</s0>
<s5>20</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Mouse</s0>
<s5>20</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Ratón</s0>
<s5>20</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Animal</s0>
<s5>21</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Caspase 3</s0>
<s2>FE</s2>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Cysteine endopeptidases</s0>
<s2>FE</s2>
<s5>45</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Cysteine endopeptidases</s0>
<s2>FE</s2>
<s5>45</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Cysteine endopeptidases</s0>
<s2>FE</s2>
<s5>45</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Enzyme</s0>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>Enzyme</s0>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Enzima</s0>
</fC07>
<fN21><s1>232</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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	Movement Disorders (revue)
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Movement Disorders (revue)

Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice

Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice

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