Inflammation-induced alteration of astrocyte mitochondrial dynamics requires autophagy for mitochondrial network maintenance.

Détails

ID Serval
serval:BIB_1EE142EBB400
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Inflammation-induced alteration of astrocyte mitochondrial dynamics requires autophagy for mitochondrial network maintenance.
Périodique
Cell Metabolism
Auteur(s)
Motori E., Puyal J., Toni N., Ghanem A., Angeloni C., Malaguti M., Cantelli-Forti G., Berninger B., Conzelmann K.K., Götz M., Winklhofer K.F., Hrelia S., Bergami M.
ISSN
1932-7420 (Electronic)
ISSN-L
1550-4131
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
18
Numéro
6
Pages
844-859
Langue
anglais
Résumé
Accumulating evidence suggests that changes in the metabolic signature of astrocytes underlie their response to neuroinflammation, but how proinflammatory stimuli induce these changes is poorly understood. By monitoring astrocytes following acute cortical injury, we identified a differential and region-specific remodeling of their mitochondrial network: while astrocytes within the penumbra of the lesion undergo mitochondrial elongation, those located in the core-the area invaded by proinflammatory cells-experience transient mitochondrial fragmentation. In brain slices, proinflammatory stimuli reproduced localized changes in mitochondrial dynamics, favoring fission over fusion. This effect was triggered by Drp1 phosphorylation and ultimately resulted in reduced respiratory capacity. Furthermore, maintenance of the mitochondrial architecture critically depended on the induction of autophagy. Deletion of Atg7, required for autophagosome formation, prevented the reestablishment of tubular mitochondria, leading to marked reactive oxygen species accumulation and cell death. Thus, our data reveal autophagy to be essential for regenerating astrocyte mitochondrial networks during inflammation.
Pubmed
Web of science
Open Access
Oui
Création de la notice
20/12/2013 10:53
Dernière modification de la notice
20/08/2019 12:54
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