ER stress inhibits neuronal death by promoting autophagy
Identifieur interne : 000464 ( Hal/Checkpoint ); précédent : 000463; suivant : 000465ER stress inhibits neuronal death by promoting autophagy
Auteurs : Antoine Fouillet [France] ; Clémence Levet [France] ; Angélique Virgone [France] ; Marion Robin [France] ; Pierre Dourlen [France] ; Jennifer Rieusset [France] ; Elise Belaidi [France] ; Michel Ovize [France] ; Monique Touret [France] ; Serge Nataf [France] ; Bertrand Mollereau [France]Source :
- Autophagy [ 1554-8627 ] ; 2012-06-01.
Descripteurs français
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.
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DOI: 10.4161
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Hal:ensl-00807628Le document en format XML
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<idno type="DOI">10.4161</idno>
<series><title level="j">Autophagy</title>
<idno type="ISSN">1554-8627</idno>
<imprint><date type="datePub">2012-06-01</date>
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<profileDesc><textClass><keywords scheme="mix" xml:lang="fr"><term>ER stress</term>
<term>apoptosis</term>
<term>autophagy</term>
<term>drosophila</term>
<term>mouse</term>
<term>parkinson</term>
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<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>
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<hal api="V3"> <titleStmt> <title xml:lang="en">ER stress inhibits neuronal death by promoting autophagy</title>
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<sourceDesc> <biblStruct> <analytic> <title xml:lang="en">ER stress inhibits neuronal death by promoting autophagy</title>
<author role="aut"> <persName> <forename type="first">Antoine</forename>
<surname>Fouillet</surname>
</persName>
<idno type="halauthorid">834110</idno>
<affiliation ref="#struct-39378"></affiliation>
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<author role="aut"> <persName> <forename type="first">Clémence</forename>
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<affiliation ref="#struct-39378"></affiliation>
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<author role="aut"> <persName> <forename type="first">Angélique</forename>
<surname>Virgone</surname>
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<affiliation ref="#struct-301088"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Marion</forename>
<surname>Robin</surname>
</persName>
<idno type="halauthorid">833840</idno>
<affiliation ref="#struct-39378"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Pierre</forename>
<surname>Dourlen</surname>
</persName>
<idno type="halauthorid">112698</idno>
<affiliation ref="#struct-39378"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Jennifer</forename>
<surname>Rieusset</surname>
</persName>
<idno type="halauthorid">834113</idno>
<affiliation ref="#struct-218708"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Elise</forename>
<surname>Belaidi</surname>
</persName>
<idno type="halauthorid">160156</idno>
<affiliation ref="#struct-218709"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Michel</forename>
<surname>Ovize</surname>
</persName>
<idno type="halauthorid">411188</idno>
<affiliation ref="#struct-218709"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Monique</forename>
<surname>Touret</surname>
</persName>
<idno type="halauthorid">834114</idno>
<affiliation ref="#struct-301088"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Serge</forename>
<surname>Nataf</surname>
</persName>
<idno type="halauthorid">156039</idno>
<affiliation ref="#struct-301088"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Bertrand</forename>
<surname>Mollereau</surname>
</persName>
<idno type="halauthorid">766018</idno>
<affiliation ref="#struct-39378"></affiliation>
</author>
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<monogr> <idno type="halJournalId" status="VALID">28676</idno>
<idno type="issn">1554-8627</idno>
<idno type="eissn">1554-8635</idno>
<title level="j">Autophagy</title>
<imprint> <publisher>Taylor & Francis</publisher>
<biblScope unit="volume">8</biblScope>
<biblScope unit="issue">6</biblScope>
<biblScope unit="pp">915 - 926</biblScope>
<date type="datePub">2012-06-01</date>
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<textClass> <keywords scheme="author"> <term xml:lang="fr">ER stress</term>
<term xml:lang="fr">autophagy</term>
<term xml:lang="fr">parkinson</term>
<term xml:lang="fr">apoptosis</term>
<term xml:lang="fr">drosophila</term>
<term xml:lang="fr">mouse</term>
</keywords>
<classCode scheme="halDomain" n="sdv.bc">Life Sciences [q-bio]/Cellular Biology</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
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<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.</abstract>
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