MovDisordV3, PascalFrancis, Corpus, bibRecord, 000484

Mortalin Inhibition in Experimental Parkinson's Disease

Identifieur interne : 000484 ( PascalFrancis/Corpus ); précédent : 000483; suivant : 000485

Mortalin Inhibition in Experimental Parkinson's Disease

Auteurs : Davide Chiasserini ; Alessandro Tozzi ; Antonio De Lure ; Michela Tantucci ; Federica Susta ; Pier Luigi Orvietani ; Keizo Koya ; Luciano Binaglia ; Paolo Calabresi

Source :

Movement disorders [ 0885-3185 ] ; 2011.

RBID : Pascal:11-0380273

Descripteurs français

Pascal (Inist)
- Maladie de Parkinson, Pathologie du système nerveux, Pathologie expérimentale, Dopamine, Mitochondrie, Protéine choc thermique.

English descriptors

KwdEn :
- Dopamine, Experimental disease, Heat shock protein, Mitochondria, Nervous system diseases, Parkinson disease.

Abstract

Among heat shock proteins, mortalin has been linked to the pathogenesis of Parkinson's disease. In the present work a rat model of Parkinson's disease was used to analyze the expression of striatal proteins and, more specifically, mortalin expression. The possible involvement of mortalin in Parkinson's disease pathogenesis was further investigated by utilizing an electrophysiological approach and pharmacological inhibition of mortalin in both the physiological and the parkinsonian states. Proteomic analysis was used to investigate changes in striatal protein expression in the 6-hydroxydopamine rat model of Parkinson's disease. The electrophysiological effects of MKT-077, a rhodamine-123 analogue acting as an inhibitor of mortalin, were measured by field potential recordings from corticostriatal brain slices obtained from control, sham-operated, and 6-hydroxydopamine-denervated animals. Slices in the presence of rotenone, an inhibitor of mitochondrial complex I, were also analyzed. Proteomic analysis revealed down-regulation of mortalin in the striata of 6-hydroxydopamine-treated rats in comparison with sham-operated animals. MKT-077 reduced corticostriatal field potential amplitude in physiological conditions, inducing membrane depolarization and inward current in striatal medium spiny neurons. In addition, we observed that concentrations of MKT-077 not inducing any electrophysiological effect in physiological conditions caused significant changes in striatal slices from parkinsonian animals as well as in slices treated with a submaximal concentration of rotenone. These findings suggest a critical link between mortalin function and mitochondrial activity in both physiological and pathological conditions mimicking Parkinson's disease.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`02`	`1`		`@1 TOZZI (Alessandro)`
A11	`03`	`1`		`@1 DE LURE (Antonio)`
A11	`04`	`1`		`@1 TANTUCCI (Michela)`
A11	`05`	`1`		`@1 SUSTA (Federica)`
A11	`06`	`1`		`@1 ORVIETANI (Pier Luigi)`
A11	`07`	`1`		`@1 KOYA (Keizo)`
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A14	`02`			`@1 Fondazione S. Lucia-I.R.C.C.S. @2 Rome @3 ITA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 9 aut.`
A14	`03`			`@1 Dipartimento di Medicina Interna, Sezione di Biochimica, Università di Perugia @2 Perugia @3 ITA @Z 5 aut. @Z 6 aut. @Z 8 aut.`
A14	`04`			`@1 Synta Pharmaceuticals Corp @2 Lexington, Massachusetts @3 USA @Z 7 aut.`
A20				`@1 1639-1647`
A21				`@1 2011`
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A44				`@0 0000 @1 © 2011 INIST-CNRS. All rights reserved.`
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C01	`01`		`ENG`	@0 Among heat shock proteins, mortalin has been linked to the pathogenesis of Parkinson's disease. In the present work a rat model of Parkinson's disease was used to analyze the expression of striatal proteins and, more specifically, mortalin expression. The possible involvement of mortalin in Parkinson's disease pathogenesis was further investigated by utilizing an electrophysiological approach and pharmacological inhibition of mortalin in both the physiological and the parkinsonian states. Proteomic analysis was used to investigate changes in striatal protein expression in the 6-hydroxydopamine rat model of Parkinson's disease. The electrophysiological effects of MKT-077, a rhodamine-123 analogue acting as an inhibitor of mortalin, were measured by field potential recordings from corticostriatal brain slices obtained from control, sham-operated, and 6-hydroxydopamine-denervated animals. Slices in the presence of rotenone, an inhibitor of mitochondrial complex I, were also analyzed. Proteomic analysis revealed down-regulation of mortalin in the striata of 6-hydroxydopamine-treated rats in comparison with sham-operated animals. MKT-077 reduced corticostriatal field potential amplitude in physiological conditions, inducing membrane depolarization and inward current in striatal medium spiny neurons. In addition, we observed that concentrations of MKT-077 not inducing any electrophysiological effect in physiological conditions caused significant changes in striatal slices from parkinsonian animals as well as in slices treated with a submaximal concentration of rotenone. These findings suggest a critical link between mortalin function and mitochondrial activity in both physiological and pathological conditions mimicking Parkinson's disease.
C02	`01`	`X`		`@0 002B17`
C02	`02`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Maladie de Parkinson @2 NM @5 01`
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C03	`04`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 10`
C03	`05`	`X`	`FRE`	`@0 Mitochondrie @5 11`
C03	`05`	`X`	`ENG`	`@0 Mitochondria @5 11`
C03	`05`	`X`	`SPA`	`@0 Mitocondria @5 11`
C03	`06`	`X`	`FRE`	`@0 Protéine choc thermique @5 12`
C03	`06`	`X`	`ENG`	`@0 Heat shock protein @5 12`
C03	`06`	`X`	`SPA`	`@0 Proteína choque térmico @5 12`
C07	`01`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 37`
C07	`01`	`X`	`ENG`	`@0 Cerebral disorder @5 37`
C07	`01`	`X`	`SPA`	`@0 Encéfalo patología @5 37`
C07	`02`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 38`
C07	`02`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 38`
C07	`02`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 38`
C07	`03`	`X`	`FRE`	`@0 Maladie dégénérative @5 39`
C07	`03`	`X`	`ENG`	`@0 Degenerative disease @5 39`
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C07	`04`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 40`
C07	`04`	`X`	`ENG`	`@0 Central nervous system disease @5 40`
C07	`04`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 40`
C07	`05`	`X`	`FRE`	`@0 Catécholamine @5 42`
C07	`05`	`X`	`ENG`	`@0 Catecholamine @5 42`
C07	`05`	`X`	`SPA`	`@0 Catecolamina @5 42`
C07	`06`	`X`	`FRE`	`@0 Neurotransmetteur @5 43`
C07	`06`	`X`	`ENG`	`@0 Neurotransmitter @5 43`
C07	`06`	`X`	`SPA`	`@0 Neurotransmisor @5 43`
N21				`@1 262`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 11-0380273 INIST
ET :	Mortalin Inhibition in Experimental Parkinson's Disease
AU :	CHIASSERINI (Davide); TOZZI (Alessandro); DE LURE (Antonio); TANTUCCI (Michela); SUSTA (Federica); ORVIETANI (Pier Luigi); KOYA (Keizo); BINAGLIA (Luciano); CALABRESI (Paolo)
AF :	Clinica Neurologica, Università degli studi di Perugia, Ospedale S. Maria della Misericordia/Perugia/Italie (1 aut., 2 aut., 3 aut., 4 aut., 9 aut.); Fondazione S. Lucia-I.R.C.C.S./Rome/Italie (1 aut., 2 aut., 3 aut., 9 aut.); Dipartimento di Medicina Interna, Sezione di Biochimica, Università di Perugia/Perugia/Italie (5 aut., 6 aut., 8 aut.); Synta Pharmaceuticals Corp/Lexington, Massachusetts/Etats-Unis (7 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2011; Vol. 26; No. 9; Pp. 1639-1647; Bibl. 53 ref.
LA :	Anglais
EA :	Among heat shock proteins, mortalin has been linked to the pathogenesis of Parkinson's disease. In the present work a rat model of Parkinson's disease was used to analyze the expression of striatal proteins and, more specifically, mortalin expression. The possible involvement of mortalin in Parkinson's disease pathogenesis was further investigated by utilizing an electrophysiological approach and pharmacological inhibition of mortalin in both the physiological and the parkinsonian states. Proteomic analysis was used to investigate changes in striatal protein expression in the 6-hydroxydopamine rat model of Parkinson's disease. The electrophysiological effects of MKT-077, a rhodamine-123 analogue acting as an inhibitor of mortalin, were measured by field potential recordings from corticostriatal brain slices obtained from control, sham-operated, and 6-hydroxydopamine-denervated animals. Slices in the presence of rotenone, an inhibitor of mitochondrial complex I, were also analyzed. Proteomic analysis revealed down-regulation of mortalin in the striata of 6-hydroxydopamine-treated rats in comparison with sham-operated animals. MKT-077 reduced corticostriatal field potential amplitude in physiological conditions, inducing membrane depolarization and inward current in striatal medium spiny neurons. In addition, we observed that concentrations of MKT-077 not inducing any electrophysiological effect in physiological conditions caused significant changes in striatal slices from parkinsonian animals as well as in slices treated with a submaximal concentration of rotenone. These findings suggest a critical link between mortalin function and mitochondrial activity in both physiological and pathological conditions mimicking Parkinson's disease.
CC :	002B17; 002B17G
FD :	Maladie de Parkinson; Pathologie du système nerveux; Pathologie expérimentale; Dopamine; Mitochondrie; Protéine choc thermique
FG :	Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Catécholamine; Neurotransmetteur
ED :	Parkinson disease; Nervous system diseases; Experimental disease; Dopamine; Mitochondria; Heat shock protein
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Catecholamine; Neurotransmitter
SD :	Parkinson enfermedad; Sistema nervioso patología; Patología experimental; Dopamina; Mitocondria; Proteína choque térmico
LO :	INIST-20953.354000508939410080
ID :	11-0380273

Links to Exploration step

Pascal:11-0380273

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Mortalin Inhibition in Experimental Parkinson's Disease</title>
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<author><name sortKey="Orvietani, Pier Luigi" sort="Orvietani, Pier Luigi" uniqKey="Orvietani P" first="Pier Luigi" last="Orvietani">Pier Luigi Orvietani</name>
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<author><name sortKey="Koya, Keizo" sort="Koya, Keizo" uniqKey="Koya K" first="Keizo" last="Koya">Keizo Koya</name>
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<series><title level="j" type="main">Movement disorders</title>
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<front><div type="abstract" xml:lang="en">Among heat shock proteins, mortalin has been linked to the pathogenesis of Parkinson's disease. In the present work a rat model of Parkinson's disease was used to analyze the expression of striatal proteins and, more specifically, mortalin expression. The possible involvement of mortalin in Parkinson's disease pathogenesis was further investigated by utilizing an electrophysiological approach and pharmacological inhibition of mortalin in both the physiological and the parkinsonian states. Proteomic analysis was used to investigate changes in striatal protein expression in the 6-hydroxydopamine rat model of Parkinson's disease. The electrophysiological effects of MKT-077, a rhodamine-123 analogue acting as an inhibitor of mortalin, were measured by field potential recordings from corticostriatal brain slices obtained from control, sham-operated, and 6-hydroxydopamine-denervated animals. Slices in the presence of rotenone, an inhibitor of mitochondrial complex I, were also analyzed. Proteomic analysis revealed down-regulation of mortalin in the striata of 6-hydroxydopamine-treated rats in comparison with sham-operated animals. MKT-077 reduced corticostriatal field potential amplitude in physiological conditions, inducing membrane depolarization and inward current in striatal medium spiny neurons. In addition, we observed that concentrations of MKT-077 not inducing any electrophysiological effect in physiological conditions caused significant changes in striatal slices from parkinsonian animals as well as in slices treated with a submaximal concentration of rotenone. These findings suggest a critical link between mortalin function and mitochondrial activity in both physiological and pathological conditions mimicking Parkinson's disease.</div>
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<ET>Mortalin Inhibition in Experimental Parkinson's Disease</ET>
<AU>CHIASSERINI (Davide); TOZZI (Alessandro); DE LURE (Antonio); TANTUCCI (Michela); SUSTA (Federica); ORVIETANI (Pier Luigi); KOYA (Keizo); BINAGLIA (Luciano); CALABRESI (Paolo)</AU>
<AF>Clinica Neurologica, Università degli studi di Perugia, Ospedale S. Maria della Misericordia/Perugia/Italie (1 aut., 2 aut., 3 aut., 4 aut., 9 aut.); Fondazione S. Lucia-I.R.C.C.S./Rome/Italie (1 aut., 2 aut., 3 aut., 9 aut.); Dipartimento di Medicina Interna, Sezione di Biochimica, Università di Perugia/Perugia/Italie (5 aut., 6 aut., 8 aut.); Synta Pharmaceuticals Corp/Lexington, Massachusetts/Etats-Unis (7 aut.)</AF>
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<EA>Among heat shock proteins, mortalin has been linked to the pathogenesis of Parkinson's disease. In the present work a rat model of Parkinson's disease was used to analyze the expression of striatal proteins and, more specifically, mortalin expression. The possible involvement of mortalin in Parkinson's disease pathogenesis was further investigated by utilizing an electrophysiological approach and pharmacological inhibition of mortalin in both the physiological and the parkinsonian states. Proteomic analysis was used to investigate changes in striatal protein expression in the 6-hydroxydopamine rat model of Parkinson's disease. The electrophysiological effects of MKT-077, a rhodamine-123 analogue acting as an inhibitor of mortalin, were measured by field potential recordings from corticostriatal brain slices obtained from control, sham-operated, and 6-hydroxydopamine-denervated animals. Slices in the presence of rotenone, an inhibitor of mitochondrial complex I, were also analyzed. Proteomic analysis revealed down-regulation of mortalin in the striata of 6-hydroxydopamine-treated rats in comparison with sham-operated animals. MKT-077 reduced corticostriatal field potential amplitude in physiological conditions, inducing membrane depolarization and inward current in striatal medium spiny neurons. In addition, we observed that concentrations of MKT-077 not inducing any electrophysiological effect in physiological conditions caused significant changes in striatal slices from parkinsonian animals as well as in slices treated with a submaximal concentration of rotenone. These findings suggest a critical link between mortalin function and mitochondrial activity in both physiological and pathological conditions mimicking Parkinson's disease.</EA>
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Movement Disorders (revue)

Mortalin Inhibition in Experimental Parkinson's Disease

Mortalin Inhibition in Experimental Parkinson's Disease

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