ER stress inhibits neuronal death by promoting autophagy.
Identifieur interne : 000861 ( PubMed/Corpus ); précédent : 000860; suivant : 000862ER stress inhibits neuronal death by promoting autophagy.
Auteurs : Antoine Fouillet ; Clemence Levet ; Angelique Virgone ; Marion Robin ; Pierre Dourlen ; Jennifer Rieusset ; Elise Belaidi ; Michel Ovize ; Monique Touret ; Serge Nataf ; Bertrand MollereauSource :
- Autophagy [ 1554-8635 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Autophagy (drug effects), Cytoprotection (drug effects), Disease Models, Animal, Drosophila melanogaster (metabolism), Endoplasmic Reticulum Stress (drug effects), Mice, Neurons (drug effects), Neurons (pathology), Neuroprotective Agents (pharmacology), Oxidopamine, Parkinson Disease (pathology), Tunicamycin (pharmacology).
- MESH :
- chemical , pharmacology : Neuroprotective Agents, Tunicamycin.
- drug effects : Autophagy, Cytoprotection, Endoplasmic Reticulum Stress, Neurons.
- metabolism : Drosophila melanogaster.
- pathology : Neurons, Parkinson Disease.
- Animals, Disease Models, Animal, Mice, Oxidopamine.
Abstract
Endoplasmic reticulum (ER) stress has been implicated in neurodegenerative diseases but its relationship and role in disease progression remain unclear. Using genetic and pharmacological approaches, we showed that mild ER stress ("preconditioning") is neuroprotective in Drosophila and mouse models of Parkinson disease. In addition, we found that the combination of mild ER stress and apoptotic signals triggers an autophagic response both in vivo and in vitro. We showed that when autophagy is impaired, ER-mediated protection is lost. We further demonstrated that autophagy inhibits caspase activation and apoptosis. Based on our findings, we conclude that autophagy is required for the neuroprotection mediated by mild ER stress, and therefore ER preconditioning has potential therapeutic value for the treatment of neurodegenerative diseases.
DOI: 10.4161/auto.19716
PubMed: 22660271
Links to Exploration step
pubmed:22660271Le document en format XML
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Dourlen</name></author><author><name sortKey="Rieusset, Jennifer" sort="Rieusset, Jennifer" uniqKey="Rieusset J" first="Jennifer" last="Rieusset">Jennifer Rieusset</name></author><author><name sortKey="Belaidi, Elise" sort="Belaidi, Elise" uniqKey="Belaidi E" first="Elise" last="Belaidi">Elise Belaidi</name></author><author><name sortKey="Ovize, Michel" sort="Ovize, Michel" uniqKey="Ovize M" first="Michel" last="Ovize">Michel Ovize</name></author><author><name sortKey="Touret, Monique" sort="Touret, Monique" uniqKey="Touret M" first="Monique" last="Touret">Monique Touret</name></author><author><name sortKey="Nataf, Serge" sort="Nataf, Serge" uniqKey="Nataf S" first="Serge" last="Nataf">Serge Nataf</name></author><author><name sortKey="Mollereau, Bertrand" sort="Mollereau, Bertrand" uniqKey="Mollereau B" first="Bertrand" last="Mollereau">Bertrand Mollereau</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno 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Virgone</name></author><author><name sortKey="Robin, Marion" sort="Robin, Marion" uniqKey="Robin M" first="Marion" last="Robin">Marion Robin</name></author><author><name sortKey="Dourlen, Pierre" sort="Dourlen, Pierre" uniqKey="Dourlen P" first="Pierre" last="Dourlen">Pierre Dourlen</name></author><author><name sortKey="Rieusset, Jennifer" sort="Rieusset, Jennifer" uniqKey="Rieusset J" first="Jennifer" last="Rieusset">Jennifer Rieusset</name></author><author><name sortKey="Belaidi, Elise" sort="Belaidi, Elise" uniqKey="Belaidi E" first="Elise" last="Belaidi">Elise Belaidi</name></author><author><name sortKey="Ovize, Michel" sort="Ovize, Michel" uniqKey="Ovize M" first="Michel" last="Ovize">Michel Ovize</name></author><author><name sortKey="Touret, Monique" sort="Touret, Monique" uniqKey="Touret M" first="Monique" last="Touret">Monique Touret</name></author><author><name sortKey="Nataf, Serge" sort="Nataf, Serge" uniqKey="Nataf S" first="Serge" last="Nataf">Serge Nataf</name></author><author><name sortKey="Mollereau, Bertrand" sort="Mollereau, Bertrand" uniqKey="Mollereau B" first="Bertrand" last="Mollereau">Bertrand Mollereau</name></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autophagy (drug effects)</term><term>Cytoprotection (drug effects)</term><term>Disease Models, Animal</term><term>Drosophila melanogaster (metabolism)</term><term>Endoplasmic Reticulum Stress (drug effects)</term><term>Mice</term><term>Neurons (drug effects)</term><term>Neurons (pathology)</term><term>Neuroprotective Agents (pharmacology)</term><term>Oxidopamine</term><term>Parkinson Disease (pathology)</term><term>Tunicamycin (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neuroprotective Agents</term><term>Tunicamycin</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cytoprotection</term><term>Endoplasmic Reticulum Stress</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Drosophila melanogaster</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Mice</term><term>Oxidopamine</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Endoplasmic reticulum (ER) stress has been implicated in neurodegenerative diseases but its relationship and role in disease progression remain unclear. Using genetic and pharmacological approaches, we showed that mild ER stress ("preconditioning") is neuroprotective in Drosophila and mouse models of Parkinson disease. In addition, we found that the combination of mild ER stress and apoptotic signals triggers an autophagic response both in vivo and in vitro. We showed that when autophagy is impaired, ER-mediated protection is lost. We further demonstrated that autophagy inhibits caspase activation and apoptosis. Based on our findings, we conclude that autophagy is required for the neuroprotection mediated by mild ER stress, and therefore ER preconditioning has potential therapeutic value for the treatment of neurodegenerative diseases.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22660271</PMID><DateCreated><Year>2012</Year><Month>08</Month><Day>24</Day></DateCreated><DateCompleted><Year>2013</Year><Month>01</Month><Day>03</Day></DateCompleted><DateRevised><Year>2015</Year><Month>02</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>6</Issue><PubDate><Year>2012</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>ER stress inhibits neuronal death by promoting autophagy.</ArticleTitle><Pagination><MedlinePgn>915-26</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4161/auto.19716</ELocationID><Abstract><AbstractText>Endoplasmic reticulum (ER) stress has been implicated in neurodegenerative diseases but its relationship and role in disease progression remain unclear. Using genetic and pharmacological approaches, we showed that mild ER stress ("preconditioning") is neuroprotective in Drosophila and mouse models of Parkinson disease. In addition, we found that the combination of mild ER stress and apoptotic signals triggers an autophagic response both in vivo and in vitro. We showed that when autophagy is impaired, ER-mediated protection is lost. We further demonstrated that autophagy inhibits caspase activation and apoptosis. Based on our findings, we conclude that autophagy is required for the neuroprotection mediated by mild ER stress, and therefore ER preconditioning has potential therapeutic value for the treatment of neurodegenerative diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fouillet</LastName><ForeName>Antoine</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Ecole Normale Supérieure de Lyon, Laboratoire de Biologie Moléculaire de la Cellule, Lyon, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Levet</LastName><ForeName>Clemence</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Virgone</LastName><ForeName>Angelique</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Robin</LastName><ForeName>Marion</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Dourlen</LastName><ForeName>Pierre</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Rieusset</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Belaidi</LastName><ForeName>Elise</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Ovize</LastName><ForeName>Michel</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Touret</LastName><ForeName>Monique</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Nataf</LastName><ForeName>Serge</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mollereau</LastName><ForeName>Bertrand</ForeName><Initials>B</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>2012</Year><Month>06</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United 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