ER stress inhibits neuronal death by promoting autophagy

被引：182

作者：

Fouillet, Antoine ^{[1
]}

Levet, Clemence ^{[1
]}

Virgone, Angelique ^{[2
]}

Robin, Marion ^{[1
]}

Dourlen, Pierre ^{[1
]}

Rieusset, Jennifer ^{[3
]}

Belaidi, Elise ^{[4
,5
]}

Ovize, Michel ^{[4
,5
]}

Touret, Monique ^{[2
]}

Nataf, Serge ^{[2
]}

Mollereau, Bertrand ^{[1
]}

机构：

[1] Ecole Normale Super Lyon, Lab Biol Mol Cellule, F-69364 Lyon, France

[2] Univ Lyon, Lyon, France

[3] Fac Med Lyon Sud, INSERM, UMR, Lyon, France

[4] Univ Lyon 1, INSERM, F-69365 Lyon, France

[5] Univ Lyon 1, Serv Explorat Fonct Cardiovasc, Hosp Civils Lyon, F-69365 Lyon, France

来源：

AUTOPHAGY | 2012年 / 8卷 / 06期

关键词：

ER stress; autophagy; Parkinson; apoptosis; Drosophila; mouse; UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM STRESS; CELL-DEATH; DROSOPHILA MODEL; SUPPRESSION; APOPTOSIS; INDUCERS; HOMOLOG; GROWTH; BRANCH;

D O I：

10.4161/auto.19716

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：915 / 926

页数：12

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