Neuroprotection by neuropeptide Y in cell and animal models of Parkinson's disease.
Identifieur interne : 000782 ( PubMed/Checkpoint ); précédent : 000781; suivant : 000783Neuroprotection by neuropeptide Y in cell and animal models of Parkinson's disease.
Auteurs : Mickael Decressac [France] ; Stéphanie Pain ; Pierre-Yves Chabeauti ; Laura Frangeul ; Nathalie Thiriet ; Herbert Herzog ; Jackie Vergote ; Sylvie Chalon ; Mohamed Jaber ; Afsaneh GaillardSource :
- Neurobiology of aging [ 1558-1497 ] ; 2012.
English descriptors
- KwdEn :
- Adrenergic Agents (toxicity), Analysis of Variance, Animals, Animals, Newborn, Arginine (analogs & derivatives), Arginine (pharmacology), Autoradiography, Cell Line, Tumor, Cell Survival (drug effects), Chromatography, High Pressure Liquid, Disease Models, Animal, Dopamine Plasma Membrane Transport Proteins (metabolism), Dopaminergic Neurons (drug effects), Dopaminergic Neurons (pathology), Enzyme Inhibitors (pharmacology), Female, Functional Laterality, Humans, MAP Kinase Signaling System (drug effects), MAP Kinase Signaling System (genetics), Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Neuroblastoma (pathology), Neurodegenerative Diseases (etiology), Neurodegenerative Diseases (genetics), Neurodegenerative Diseases (prevention & control), Neuropeptide Y (therapeutic use), Neuroprotective Agents (therapeutic use), Nortropanes (pharmacokinetics), Oligopeptides (therapeutic use), Oxidopamine (toxicity), Parkinson Disease (complications), Parkinson Disease (etiology), Parkinson Disease (prevention & control), Protein Binding (drug effects), Protein Binding (genetics), Rats, Rats, Wistar, Receptors, Neuropeptide Y (agonists), Receptors, Neuropeptide Y (antagonists & inhibitors), Receptors, Neuropeptide Y (deficiency), Substantia Nigra (drug effects), Substantia Nigra (pathology), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , agonists : Receptors, Neuropeptide Y.
- chemical , analogs & derivatives : Arginine.
- chemical , antagonists & inhibitors : Receptors, Neuropeptide Y.
- chemical , deficiency : Receptors, Neuropeptide Y.
- chemical , metabolism : Dopamine Plasma Membrane Transport Proteins, Tyrosine 3-Monooxygenase.
- chemical , pharmacokinetics : Nortropanes.
- chemical , pharmacology : Arginine, Enzyme Inhibitors.
- chemical , therapeutic use : Neuropeptide Y, Neuroprotective Agents, Oligopeptides.
- chemical , toxicity : Adrenergic Agents, Oxidopamine.
- complications : Parkinson Disease.
- drug effects : Cell Survival, Dopaminergic Neurons, MAP Kinase Signaling System, Protein Binding, Substantia Nigra.
- etiology : Neurodegenerative Diseases, Parkinson Disease.
- genetics : MAP Kinase Signaling System, Neurodegenerative Diseases, Protein Binding.
- pathology : Dopaminergic Neurons, Neuroblastoma, Substantia Nigra.
- prevention & control : Neurodegenerative Diseases, Parkinson Disease.
- Analysis of Variance, Animals, Animals, Newborn, Autoradiography, Cell Line, Tumor, Chromatography, High Pressure Liquid, Disease Models, Animal, Female, Functional Laterality, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Rats, Rats, Wistar.
Abstract
This study was aimed to investigate the potential neuroprotective effect of neuropeptide Y (NPY) on the survival of dopaminergic cells in both in vitro and in animal models of Parkinson's disease (PD). NPY protected human SH-SY5Y dopaminergic neuroblastoma cells from 6-hydroxydopamine-induced toxicity. In rat and mice models of PD, striatal injection of NPY preserved the nigrostriatal dopamine pathway from degeneration as evidenced by quantification of (1) tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta, levels of (2) striatal tyrosine hydroxylase and dopamine transporter, (3) dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) as well as (4) rotational behavior. NPY had no neuroprotective effects in mice treated with Y(2) receptor antagonist or in transgenic mice deficient for Y(2) receptor suggesting that NPY effects are mediated through this receptor. Stimulation of Y(2) receptor by NPY triggered the activation of both the ERK1/2 and Akt pathways but did not modify levels of brain derived neurotrophic factor (BDNF) or glial cell line-derived neurotrophic factor. These results open new perspectives in neuroprotective therapies using NPY and suggest potential beneficial effects in PD.
DOI: 10.1016/j.neurobiolaging.2011.06.018
PubMed: 21816512
Affiliations:
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Tumor</term><term>Chromatography, High Pressure Liquid</term><term>Disease Models, Animal</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This study was aimed to investigate the potential neuroprotective effect of neuropeptide Y (NPY) on the survival of dopaminergic cells in both in vitro and in animal models of Parkinson's disease (PD). NPY protected human SH-SY5Y dopaminergic neuroblastoma cells from 6-hydroxydopamine-induced toxicity. In rat and mice models of PD, striatal injection of NPY preserved the nigrostriatal dopamine pathway from degeneration as evidenced by quantification of (1) tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta, levels of (2) striatal tyrosine hydroxylase and dopamine transporter, (3) dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) as well as (4) rotational behavior. NPY had no neuroprotective effects in mice treated with Y(2) receptor antagonist or in transgenic mice deficient for Y(2) receptor suggesting that NPY effects are mediated through this receptor. Stimulation of Y(2) receptor by NPY triggered the activation of both the ERK1/2 and Akt pathways but did not modify levels of brain derived neurotrophic factor (BDNF) or glial cell line-derived neurotrophic factor. These results open new perspectives in neuroprotective therapies using NPY and suggest potential beneficial effects in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21816512</PMID><DateCreated><Year>2012</Year><Month>07</Month><Day>06</Day></DateCreated><DateCompleted><Year>2012</Year><Month>11</Month><Day>29</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1558-1497</ISSN><JournalIssue CitedMedium="Internet"><Volume>33</Volume><Issue>9</Issue><PubDate><Year>2012</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Neurobiology of aging</Title><ISOAbbreviation>Neurobiol. Aging</ISOAbbreviation></Journal><ArticleTitle>Neuroprotection by neuropeptide Y in cell and animal models of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>2125-37</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neurobiolaging.2011.06.018</ELocationID><Abstract><AbstractText>This study was aimed to investigate the potential neuroprotective effect of neuropeptide Y (NPY) on the survival of dopaminergic cells in both in vitro and in animal models of Parkinson's disease (PD). NPY protected human SH-SY5Y dopaminergic neuroblastoma cells from 6-hydroxydopamine-induced toxicity. In rat and mice models of PD, striatal injection of NPY preserved the nigrostriatal dopamine pathway from degeneration as evidenced by quantification of (1) tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta, levels of (2) striatal tyrosine hydroxylase and dopamine transporter, (3) dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) as well as (4) rotational behavior. NPY had no neuroprotective effects in mice treated with Y(2) receptor antagonist or in transgenic mice deficient for Y(2) receptor suggesting that NPY effects are mediated through this receptor. Stimulation of Y(2) receptor by NPY triggered the activation of both the ERK1/2 and Akt pathways but did not modify levels of brain derived neurotrophic factor (BDNF) or glial cell line-derived neurotrophic factor. These results open new perspectives in neuroprotective therapies using NPY and suggest potential beneficial effects in PD.</AbstractText><CopyrightInformation>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Decressac</LastName><ForeName>Mickael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, Centre National de la Recherche Scientifique (CNRS), Poitiers, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pain</LastName><ForeName>Stéphanie</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Chabeauti</LastName><ForeName>Pierre-Yves</ForeName><Initials>PY</Initials></Author><Author ValidYN="Y"><LastName>Frangeul</LastName><ForeName>Laura</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Thiriet</LastName><ForeName>Nathalie</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Herzog</LastName><ForeName>Herbert</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Vergote</LastName><ForeName>Jackie</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Chalon</LastName><ForeName>Sylvie</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Jaber</LastName><ForeName>Mohamed</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Gaillard</LastName><ForeName>Afsaneh</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>08</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Aging</MedlineTA><NlmUniqueID>8100437</NlmUniqueID><ISSNLinking>0197-4580</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018663">Adrenergic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C092926">BIBP 3226</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050483">Dopamine Plasma Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C113010">N-(3-iodoprop-2-enyl)-2-beta-carbomethoxy-3-(4-methylphenyl)nortropane</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009478">Neuropeptide Y</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009662">Nortropanes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009842">Oligopeptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017476">Receptors, Neuropeptide Y</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C097212">neuropeptide Y-Y1 receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C095889">neuropeptide Y2 receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance UI="D016627">Oxidopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>94ZLA3W45F</RegistryNumber><NameOfSubstance UI="D001120">Arginine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 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UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017476" MajorTopicYN="N">Receptors, Neuropeptide Y</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>03</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>06</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>06</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>12</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21816512</ArticleId><ArticleId IdType="pii">S0197-4580(11)00235-1</ArticleId><ArticleId IdType="doi">10.1016/j.neurobiolaging.2011.06.018</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Nouvelle-Aquitaine</li><li>Poitou-Charentes</li></region><settlement><li>Poitiers</li></settlement><orgName><li>Université de Poitiers</li></orgName></list><tree><noCountry><name sortKey="Chabeauti, Pierre Yves" sort="Chabeauti, Pierre Yves" uniqKey="Chabeauti P" first="Pierre-Yves" last="Chabeauti">Pierre-Yves Chabeauti</name><name sortKey="Chalon, Sylvie" sort="Chalon, Sylvie" uniqKey="Chalon S" first="Sylvie" last="Chalon">Sylvie Chalon</name><name sortKey="Frangeul, Laura" sort="Frangeul, Laura" uniqKey="Frangeul L" first="Laura" last="Frangeul">Laura Frangeul</name><name sortKey="Gaillard, Afsaneh" sort="Gaillard, Afsaneh" uniqKey="Gaillard A" first="Afsaneh" last="Gaillard">Afsaneh Gaillard</name><name sortKey="Herzog, Herbert" sort="Herzog, Herbert" uniqKey="Herzog H" first="Herbert" last="Herzog">Herbert Herzog</name><name sortKey="Jaber, Mohamed" sort="Jaber, Mohamed" uniqKey="Jaber M" first="Mohamed" last="Jaber">Mohamed Jaber</name><name sortKey="Pain, Stephanie" sort="Pain, Stephanie" uniqKey="Pain S" first="Stéphanie" last="Pain">Stéphanie Pain</name><name sortKey="Thiriet, Nathalie" sort="Thiriet, Nathalie" uniqKey="Thiriet N" first="Nathalie" last="Thiriet">Nathalie Thiriet</name><name sortKey="Vergote, Jackie" sort="Vergote, Jackie" uniqKey="Vergote J" first="Jackie" last="Vergote">Jackie Vergote</name></noCountry><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Decressac, Mickael" sort="Decressac, Mickael" uniqKey="Decressac M" first="Mickael" last="Decressac">Mickael Decressac</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Neuroprotection by neuropeptide Y in cell and animal models of Parkinson's disease.
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