ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000236

Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease

Identifieur interne : 000236 ( PascalFrancis/Corpus ); précédent : 000235; suivant : 000237

Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease

Auteurs : S. Al Sweidi ; M. G. Sanchez ; M. Bourque ; M. Morissette ; D. Dluzen ; T. Di Paolo

Source :

Journal of neuroendocrinology [ 0953-8194 ] ; 2012.

RBID : Pascal:12-0056897

Descripteurs français

Pascal (Inist)
- Oestrogène, Récepteur biologique, Stéroïde, Neurotoxine, 17β-Oestradiol, Dopamine, Maladie de Parkinson, Protéine transport, Akt protein kinase, Glycogen synthase kinase-3β, MPTP.

English descriptors

KwdEn :
- 17β-Estradiol, Akt protein kinase, Biological receptor, Carrier protein, Dopamine, Estrogen, Glycogen synthase kinase-3β, Neurotoxin, Parkinson disease, Steroid.

Abstract

Parkinson's disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17β-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)α and β distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57BI/6 male mice. Intact ERKOβ mice had lower levels of striatal DAT and VMAT2, whereas ERKOα mice were the most sensitive to MPTP toxicity compared to WT and ERKOβ mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17β-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17β-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17β-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/βIII-tubulin, pGSK3 (Ser 9)/βIII-tubulin and Akt/βIII-tubulin. Hence, ERα, ERβ and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0953-8194`
A03		`1`		`@0 J. neuroendocrinol.`
A05				`@2 24`
A06				`@2 1`
A08	`01`	`1`	`ENG`	`@1 Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease`
A09	`01`	`1`	`ENG`	`@1 Steroids and the Nervous System`
A11	`01`	`1`		`@1 AL SWEIDI (S.)`
A11	`02`	`1`		`@1 SANCHEZ (M. G.)`
A11	`03`	`1`		`@1 BOURQUE (M.)`
A11	`04`	`1`		`@1 MORISSETTE (M.)`
A11	`05`	`1`		`@1 DLUZEN (D.)`
A11	`06`	`1`		`@1 DI PAOLO (T.)`
A12	`01`	`1`		`@1 PANZICA (GianCarlo) @9 ed.`
A12	`02`	`1`		`@1 MELCANGI (Roberto C.) @9 ed.`
A14	`01`			`@1 Molecular Endocrinology and Genomic Research Center, CHUO (CHUL) @2 Quebec City @3 CAN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 6 aut.`
A14	`02`			`@1 Faculty of Pharmacy, Laval University @2 Quebec City @3 CAN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 6 aut.`
A14	`03`			`@1 Department of Anatomy and Neurobiology, Northeastern Ohio Universities College of Medicine and Pharmacy (NEOUCOM) @2 Rootstown, OH @3 USA @Z 5 aut.`
A15	`01`			`@1 Laboratory of Neuroendocrinology, Department of Anatomy, Pharmacology and Forensic Medicine, Neuroscience Institute of Turin (NIT), University of Torino @2 Torino @3 ITA @Z 1 aut.`
A15	`02`			`@1 Neuroscience Institute Cavalieri-Ottolenghi (NICO) @2 Orbassano @3 ITA @Z 1 aut.`
A15	`03`			`@1 Department of Endocrinology, Pathophysiology and Applied Biology- Center of Excellence on Neurodegenrative Diseases, University of Milano @2 Milano @3 ITA @Z 2 aut.`
A20				`@1 48-61`
A21				`@1 2012`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 22091 @5 354000505963040040`
A44				`@0 0000 @1 © 2012 INIST-CNRS. All rights reserved.`
A45				`@0 166 ref.`
A47	`01`	`1`		`@0 12-0056897`
A60				`@1 P @2 C`
A61				`@0 A`
A64	`01`	`1`		`@0 Journal of neuroendocrinology`
A66	`01`			`@0 GBR`
C01	`01`		`ENG`	@0 Parkinson's disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17β-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)α and β distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57BI/6 male mice. Intact ERKOβ mice had lower levels of striatal DAT and VMAT2, whereas ERKOα mice were the most sensitive to MPTP toxicity compared to WT and ERKOβ mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17β-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17β-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17β-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/βIII-tubulin, pGSK3 (Ser 9)/βIII-tubulin and Akt/βIII-tubulin. Hence, ERα, ERβ and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.
C02	`01`	`X`		`@0 002A28`
C02	`02`	`X`		`@0 002B17G`
C02	`03`	`X`		`@0 002B17A01`
C03	`01`	`X`	`FRE`	`@0 Oestrogène @5 01`
C03	`01`	`X`	`ENG`	`@0 Estrogen @5 01`
C03	`01`	`X`	`SPA`	`@0 Estrógeno @5 01`
C03	`02`	`X`	`FRE`	`@0 Récepteur biologique @5 02`
C03	`02`	`X`	`ENG`	`@0 Biological receptor @5 02`
C03	`02`	`X`	`SPA`	`@0 Receptor biológico @5 02`
C03	`03`	`X`	`FRE`	`@0 Stéroïde @5 03`
C03	`03`	`X`	`ENG`	`@0 Steroid @5 03`
C03	`03`	`X`	`SPA`	`@0 Esteroide @5 03`
C03	`04`	`X`	`FRE`	`@0 Neurotoxine @5 04`
C03	`04`	`X`	`ENG`	`@0 Neurotoxin @5 04`
C03	`04`	`X`	`SPA`	`@0 Neurotoxina @5 04`
C03	`05`	`X`	`FRE`	`@0 17β-Oestradiol @2 NK @5 07`
C03	`05`	`X`	`ENG`	`@0 17β-Estradiol @2 NK @5 07`
C03	`05`	`X`	`SPA`	`@0 17β-Estradiol @2 NK @5 07`
C03	`06`	`X`	`FRE`	`@0 Dopamine @2 NK @2 FR @5 08`
C03	`06`	`X`	`ENG`	`@0 Dopamine @2 NK @2 FR @5 08`
C03	`06`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 08`
C03	`07`	`X`	`FRE`	`@0 Maladie de Parkinson @2 NM @5 09`
C03	`07`	`X`	`ENG`	`@0 Parkinson disease @2 NM @5 09`
C03	`07`	`X`	`SPA`	`@0 Parkinson enfermedad @2 NM @5 09`
C03	`08`	`X`	`FRE`	`@0 Protéine transport @5 13`
C03	`08`	`X`	`ENG`	`@0 Carrier protein @5 13`
C03	`08`	`X`	`SPA`	`@0 Proteína transportador @5 13`
C03	`09`	`X`	`FRE`	`@0 Akt protein kinase @2 FE @5 14`
C03	`09`	`X`	`ENG`	`@0 Akt protein kinase @2 FE @5 14`
C03	`09`	`X`	`SPA`	`@0 Akt protein kinase @2 FE @5 14`
C03	`10`	`X`	`FRE`	`@0 Glycogen synthase kinase-3β @2 FE @5 15`
C03	`10`	`X`	`ENG`	`@0 Glycogen synthase kinase-3β @2 FE @5 15`
C03	`10`	`X`	`SPA`	`@0 Glycogen synthase kinase-3β @2 FE @5 15`
C03	`11`	`X`	`FRE`	`@0 MPTP @4 INC @5 76`
C07	`01`	`X`	`FRE`	`@0 Toxine`
C07	`01`	`X`	`ENG`	`@0 Toxin`
C07	`01`	`X`	`SPA`	`@0 Toxina`
C07	`02`	`X`	`FRE`	`@0 Transferases @2 FE`
C07	`02`	`X`	`ENG`	`@0 Transferases @2 FE`
C07	`02`	`X`	`SPA`	`@0 Transferases @2 FE`
C07	`03`	`X`	`FRE`	`@0 Enzyme @2 FE`
C07	`03`	`X`	`ENG`	`@0 Enzyme @2 FE`
C07	`03`	`X`	`SPA`	`@0 Enzima @2 FE`
C07	`04`	`X`	`FRE`	`@0 Hormone ovarienne @5 20`
C07	`04`	`X`	`ENG`	`@0 Ovarian hormone @5 20`
C07	`04`	`X`	`SPA`	`@0 Hormona ovárica @5 20`
C07	`05`	`X`	`FRE`	`@0 Hormone stéroïde sexuelle @5 21`
C07	`05`	`X`	`ENG`	`@0 Sex steroid hormone @5 21`
C07	`05`	`X`	`SPA`	`@0 Hormona esteroide sexual @5 21`
C07	`06`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 22`
C07	`06`	`X`	`ENG`	`@0 Cerebral disorder @5 22`
C07	`06`	`X`	`SPA`	`@0 Encéfalo patología @5 22`
C07	`07`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 23`
C07	`07`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 23`
C07	`07`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 23`
C07	`08`	`X`	`FRE`	`@0 Maladie dégénérative @5 24`
C07	`08`	`X`	`ENG`	`@0 Degenerative disease @5 24`
C07	`08`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 24`
C07	`09`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 25`
C07	`09`	`X`	`ENG`	`@0 Central nervous system disease @5 25`
C07	`09`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 25`
C07	`10`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 26`
C07	`10`	`X`	`ENG`	`@0 Nervous system diseases @5 26`
C07	`10`	`X`	`SPA`	`@0 Sistema nervioso patología @5 26`
C07	`11`	`X`	`FRE`	`@0 Catécholamine @5 27`
C07	`11`	`X`	`ENG`	`@0 Catecholamine @5 27`
C07	`11`	`X`	`SPA`	`@0 Catecolamina @5 27`
C07	`12`	`X`	`FRE`	`@0 Neurotransmetteur @5 28`
C07	`12`	`X`	`ENG`	`@0 Neurotransmitter @5 28`
C07	`12`	`X`	`SPA`	`@0 Neurotransmisor @5 28`
N21				`@1 037`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

A30	`01`	`1`	`ENG`	`@1 International Steroids and the Nervous System Meeting @2 6 @3 Turin ITA @4 2011-02-19`

Format Inist (serveur)

NO :	PASCAL 12-0056897 INIST
ET :	Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease
AU :	AL SWEIDI (S.); SANCHEZ (M. G.); BOURQUE (M.); MORISSETTE (M.); DLUZEN (D.); DI PAOLO (T.); PANZICA (GianCarlo); MELCANGI (Roberto C.)
AF :	Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)/Quebec City/Canada (1 aut., 2 aut., 3 aut., 4 aut., 6 aut.); Faculty of Pharmacy, Laval University/Quebec City/Canada (1 aut., 2 aut., 3 aut., 6 aut.); Department of Anatomy and Neurobiology, Northeastern Ohio Universities College of Medicine and Pharmacy (NEOUCOM)/Rootstown, OH/Etats-Unis (5 aut.); Laboratory of Neuroendocrinology, Department of Anatomy, Pharmacology and Forensic Medicine, Neuroscience Institute of Turin (NIT), University of Torino/Torino/Italie (1 aut.); Neuroscience Institute Cavalieri-Ottolenghi (NICO)/Orbassano/Italie (1 aut.); Department of Endocrinology, Pathophysiology and Applied Biology- Center of Excellence on Neurodegenrative Diseases, University of Milano/Milano/Italie (2 aut.)
DT :	Publication en série; Congrès; Niveau analytique
SO :	Journal of neuroendocrinology; ISSN 0953-8194; Royaume-Uni; Da. 2012; Vol. 24; No. 1; Pp. 48-61; Bibl. 166 ref.
LA :	Anglais
EA :	Parkinson's disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17β-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)α and β distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57BI/6 male mice. Intact ERKOβ mice had lower levels of striatal DAT and VMAT2, whereas ERKOα mice were the most sensitive to MPTP toxicity compared to WT and ERKOβ mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17β-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17β-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17β-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/βIII-tubulin, pGSK3 (Ser 9)/βIII-tubulin and Akt/βIII-tubulin. Hence, ERα, ERβ and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.
CC :	002A28; 002B17G; 002B17A01
FD :	Oestrogène; Récepteur biologique; Stéroïde; Neurotoxine; 17β-Oestradiol; Dopamine; Maladie de Parkinson; Protéine transport; Akt protein kinase; Glycogen synthase kinase-3β; MPTP
FG :	Toxine; Transferases; Enzyme; Hormone ovarienne; Hormone stéroïde sexuelle; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux; Catécholamine; Neurotransmetteur
ED :	Estrogen; Biological receptor; Steroid; Neurotoxin; 17β-Estradiol; Dopamine; Parkinson disease; Carrier protein; Akt protein kinase; Glycogen synthase kinase-3β
EG :	Toxin; Transferases; Enzyme; Ovarian hormone; Sex steroid hormone; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Catecholamine; Neurotransmitter
SD :	Estrógeno; Receptor biológico; Esteroide; Neurotoxina; 17β-Estradiol; Dopamina; Parkinson enfermedad; Proteína transportador; Akt protein kinase; Glycogen synthase kinase-3β
LO :	INIST-22091.354000505963040040
ID :	12-0056897

Links to Exploration step

Pascal:12-0056897

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease</title>
<author><name sortKey="Al Sweidi, S" sort="Al Sweidi, S" uniqKey="Al Sweidi S" first="S." last="Al Sweidi">S. Al Sweidi</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sanchez, M G" sort="Sanchez, M G" uniqKey="Sanchez M" first="M. G." last="Sanchez">M. G. Sanchez</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bourque, M" sort="Bourque, M" uniqKey="Bourque M" first="M." last="Bourque">M. Bourque</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Morissette, M" sort="Morissette, M" uniqKey="Morissette M" first="M." last="Morissette">M. Morissette</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Dluzen, D" sort="Dluzen, D" uniqKey="Dluzen D" first="D." last="Dluzen">D. Dluzen</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Anatomy and Neurobiology, Northeastern Ohio Universities College of Medicine and Pharmacy (NEOUCOM)</s1>
<s2>Rootstown, OH</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Di Paolo, T" sort="Di Paolo, T" uniqKey="Di Paolo T" first="T." last="Di Paolo">T. Di Paolo</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">12-0056897</idno>
<date when="2012">2012</date>
<idno type="stanalyst">PASCAL 12-0056897 INIST</idno>
<idno type="RBID">Pascal:12-0056897</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000236</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease</title>
<author><name sortKey="Al Sweidi, S" sort="Al Sweidi, S" uniqKey="Al Sweidi S" first="S." last="Al Sweidi">S. Al Sweidi</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sanchez, M G" sort="Sanchez, M G" uniqKey="Sanchez M" first="M. G." last="Sanchez">M. G. Sanchez</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bourque, M" sort="Bourque, M" uniqKey="Bourque M" first="M." last="Bourque">M. Bourque</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Morissette, M" sort="Morissette, M" uniqKey="Morissette M" first="M." last="Morissette">M. Morissette</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Dluzen, D" sort="Dluzen, D" uniqKey="Dluzen D" first="D." last="Dluzen">D. Dluzen</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Anatomy and Neurobiology, Northeastern Ohio Universities College of Medicine and Pharmacy (NEOUCOM)</s1>
<s2>Rootstown, OH</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Di Paolo, T" sort="Di Paolo, T" uniqKey="Di Paolo T" first="T." last="Di Paolo">T. Di Paolo</name>
<affiliation><inist:fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Journal of neuroendocrinology</title>
<title level="j" type="abbreviated">J. neuroendocrinol.</title>
<idno type="ISSN">0953-8194</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Journal of neuroendocrinology</title>
<title level="j" type="abbreviated">J. neuroendocrinol.</title>
<idno type="ISSN">0953-8194</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>17β-Estradiol</term>
<term>Akt protein kinase</term>
<term>Biological receptor</term>
<term>Carrier protein</term>
<term>Dopamine</term>
<term>Estrogen</term>
<term>Glycogen synthase kinase-3β</term>
<term>Neurotoxin</term>
<term>Parkinson disease</term>
<term>Steroid</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Oestrogène</term>
<term>Récepteur biologique</term>
<term>Stéroïde</term>
<term>Neurotoxine</term>
<term>17β-Oestradiol</term>
<term>Dopamine</term>
<term>Maladie de Parkinson</term>
<term>Protéine transport</term>
<term>Akt protein kinase</term>
<term>Glycogen synthase kinase-3β</term>
<term>MPTP</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17β-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)α and β distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57BI/6 male mice. Intact ERKOβ mice had lower levels of striatal DAT and VMAT2, whereas ERKOα mice were the most sensitive to MPTP toxicity compared to WT and ERKOβ mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17β-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17β-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17β-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/βIII-tubulin, pGSK3 (Ser 9)/βIII-tubulin and Akt/βIII-tubulin. Hence, ERα, ERβ and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0953-8194</s0>
</fA01>
<fA03 i2="1"><s0>J. neuroendocrinol.</s0>
</fA03>
<fA05><s2>24</s2>
</fA05>
<fA06><s2>1</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease</s1>
</fA08>
<fA09 i1="01" i2="1" l="ENG"><s1>Steroids and the Nervous System</s1>
</fA09>
<fA11 i1="01" i2="1"><s1>AL SWEIDI (S.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>SANCHEZ (M. G.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>BOURQUE (M.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>MORISSETTE (M.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>DLUZEN (D.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>DI PAOLO (T.)</s1>
</fA11>
<fA12 i1="01" i2="1"><s1>PANZICA (GianCarlo)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="02" i2="1"><s1>MELCANGI (Roberto C.)</s1>
<s9>ed.</s9>
</fA12>
<fA14 i1="01"><s1>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Quebec City</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Anatomy and Neurobiology, Northeastern Ohio Universities College of Medicine and Pharmacy (NEOUCOM)</s1>
<s2>Rootstown, OH</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA15 i1="01"><s1>Laboratory of Neuroendocrinology, Department of Anatomy, Pharmacology and Forensic Medicine, Neuroscience Institute of Turin (NIT), University of Torino</s1>
<s2>Torino</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="02"><s1>Neuroscience Institute Cavalieri-Ottolenghi (NICO)</s1>
<s2>Orbassano</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="03"><s1>Department of Endocrinology, Pathophysiology and Applied Biology- Center of Excellence on Neurodegenrative Diseases, University of Milano</s1>
<s2>Milano</s2>
<s3>ITA</s3>
<sZ>2 aut.</sZ>
</fA15>
<fA20><s1>48-61</s1>
</fA20>
<fA21><s1>2012</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>22091</s2>
<s5>354000505963040040</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>166 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>12-0056897</s0>
</fA47>
<fA60><s1>P</s1>
<s2>C</s2>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Journal of neuroendocrinology</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Parkinson's disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17β-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)α and β distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57BI/6 male mice. Intact ERKOβ mice had lower levels of striatal DAT and VMAT2, whereas ERKOα mice were the most sensitive to MPTP toxicity compared to WT and ERKOβ mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17β-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17β-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17β-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/βIII-tubulin, pGSK3 (Ser 9)/βIII-tubulin and Akt/βIII-tubulin. Hence, ERα, ERβ and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A28</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B17A01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Oestrogène</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Estrogen</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Estrógeno</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Récepteur biologique</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Biological receptor</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Receptor biológico</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Stéroïde</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Steroid</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Esteroide</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Neurotoxine</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Neurotoxin</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Neurotoxina</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>17β-Oestradiol</s0>
<s2>NK</s2>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>17β-Estradiol</s0>
<s2>NK</s2>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>17β-Estradiol</s0>
<s2>NK</s2>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Protéine transport</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Carrier protein</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Proteína transportador</s0>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Akt protein kinase</s0>
<s2>FE</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Akt protein kinase</s0>
<s2>FE</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Akt protein kinase</s0>
<s2>FE</s2>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Glycogen synthase kinase-3β</s0>
<s2>FE</s2>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Glycogen synthase kinase-3β</s0>
<s2>FE</s2>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Glycogen synthase kinase-3β</s0>
<s2>FE</s2>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>MPTP</s0>
<s4>INC</s4>
<s5>76</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Toxine</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Toxin</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Toxina</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Hormone ovarienne</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Ovarian hormone</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Hormona ovárica</s0>
<s5>20</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Hormone stéroïde sexuelle</s0>
<s5>21</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Sex steroid hormone</s0>
<s5>21</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Hormona esteroide sexual</s0>
<s5>21</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>22</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>22</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>23</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>24</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>24</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>25</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>25</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>25</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Pathologie du   système nerveux</s0>
<s5>26</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>26</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>26</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>27</s5>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>27</s5>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>27</s5>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>28</s5>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>28</s5>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>28</s5>
</fC07>
<fN21><s1>037</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
<pR><fA30 i1="01" i2="1" l="ENG"><s1>International Steroids and the Nervous System Meeting</s1>
<s2>6</s2>
<s3>Turin ITA</s3>
<s4>2011-02-19</s4>
</fA30>
</pR>
</standard>
<server><NO>PASCAL 12-0056897 INIST</NO>
<ET>Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease</ET>
<AU>AL SWEIDI (S.); SANCHEZ (M. G.); BOURQUE (M.); MORISSETTE (M.); DLUZEN (D.); DI PAOLO (T.); PANZICA (GianCarlo); MELCANGI (Roberto C.)</AU>
<AF>Molecular Endocrinology and Genomic Research Center, CHUO (CHUL)/Quebec City/Canada (1 aut., 2 aut., 3 aut., 4 aut., 6 aut.); Faculty of Pharmacy, Laval University/Quebec City/Canada (1 aut., 2 aut., 3 aut., 6 aut.); Department of Anatomy and Neurobiology, Northeastern Ohio Universities College of Medicine and Pharmacy (NEOUCOM)/Rootstown, OH/Etats-Unis (5 aut.); Laboratory of Neuroendocrinology, Department of Anatomy, Pharmacology and Forensic Medicine, Neuroscience Institute of Turin (NIT), University of Torino/Torino/Italie (1 aut.); Neuroscience Institute Cavalieri-Ottolenghi (NICO)/Orbassano/Italie (1 aut.); Department of Endocrinology, Pathophysiology and Applied Biology- Center of Excellence on Neurodegenrative Diseases, University of Milano/Milano/Italie (2 aut.)</AF>
<DT>Publication en série; Congrès; Niveau analytique</DT>
<SO>Journal of neuroendocrinology; ISSN 0953-8194; Royaume-Uni; Da. 2012; Vol. 24; No. 1; Pp. 48-61; Bibl. 166 ref.</SO>
<LA>Anglais</LA>
<EA>Parkinson's disease (PD) is an age-related neurodegenerative disorder with a higher incidence in the male population. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 17β-oestradiol but not androgens were shown to protect dopamine (DA) neurones. We report that oestrogen receptors (ER)α and β distinctly contribute to neuroprotection against MPTP toxicity, as revealed by examining the membrane DA transporter (DAT), the vesicular monoamine transporter 2 (VMAT2) and tyrosine hyroxylase in ER wild-type (WT) and knockout (ERKO) C57BI/6 male mice. Intact ERKOβ mice had lower levels of striatal DAT and VMAT2, whereas ERKOα mice were the most sensitive to MPTP toxicity compared to WT and ERKOβ mice and had the highest levels of plasma androgens. In both ERKO mice groups, treatment with 17β-oestradiol did not provide neuroprotection against MPTP, despite elevated plasma 17β-oestradiol levels. Next, the recently described membrane G protein-coupled oestrogen receptor (GPER1) was examined in female Macaca fascicularis monkeys and mice. GPER1 levels were increased in the caudate nucleus and the putamen of MPTP-monkeys and in the male mouse striatum lesioned with methamphetamine or MPTP. Moreover, neuroprotective mechanisms in response to oestrogens transmit via Akt/glycogen synthase kinase-3 (GSK3) signalling. The intact and lesioned striata of 17β-oestradiol treated monkeys, similar to that of mice, had increased levels of pAkt (Ser 473)/βIII-tubulin, pGSK3 (Ser 9)/βIII-tubulin and Akt/βIII-tubulin. Hence, ERα, ERβ and GPER1 activation by oestrogens is imperative in the modulation of ER signalling and serves as a basis for evaluating nigrostriatal neuroprotection.</EA>
<CC>002A28; 002B17G; 002B17A01</CC>
<FD>Oestrogène; Récepteur biologique; Stéroïde; Neurotoxine; 17β-Oestradiol; Dopamine; Maladie de Parkinson; Protéine transport; Akt protein kinase; Glycogen synthase kinase-3β; MPTP</FD>
<FG>Toxine; Transferases; Enzyme; Hormone ovarienne; Hormone stéroïde sexuelle; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central; Pathologie du système nerveux; Catécholamine; Neurotransmetteur</FG>
<ED>Estrogen; Biological receptor; Steroid; Neurotoxin; 17β-Estradiol; Dopamine; Parkinson disease; Carrier protein; Akt protein kinase; Glycogen synthase kinase-3β</ED>
<EG>Toxin; Transferases; Enzyme; Ovarian hormone; Sex steroid hormone; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Catecholamine; Neurotransmitter</EG>
<SD>Estrógeno; Receptor biológico; Esteroide; Neurotoxina; 17β-Estradiol; Dopamina; Parkinson enfermedad; Proteína transportador; Akt protein kinase; Glycogen synthase kinase-3β</SD>
<LO>INIST-22091.354000505963040040</LO>
<ID>12-0056897</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/PascalFrancis/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000236 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000236 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Canada
   |area=    ParkinsonCanadaV1
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:12-0056897
   |texte=   Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease
}}

This area was generated with Dilib version V0.6.29.
Data generation: Thu May 4 22:20:19 2017. Site generation: Fri Dec 23 23:17:26 2022

	La maladie de Parkinson au Canada (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.

La maladie de Parkinson au Canada (serveur d'exploration)

Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease

Oestrogen Receptors and Signalling Pathways: Implications for Neuroprotective Effects of Sex Steroids in Parkinson's Disease

Source :

Descripteurs français

English descriptors

Abstract

Notice en format standard (ISO 2709)

Format Inist (serveur)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri