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000137156 0247_ $$2doi$$a10.1016/j.cmet.2013.11.005
000137156 0247_ $$2pmid$$apmid:24315370
000137156 0247_ $$2ISSN$$a1550-4131
000137156 0247_ $$2ISSN$$a1932-7420
000137156 0247_ $$2altmetric$$aaltmetric:1967201
000137156 037__ $$aDZNE-2020-03478
000137156 041__ $$aEnglish
000137156 082__ $$a570
000137156 1001_ $$0P:(DE-HGF)0$$aMotori, Elisa$$b0$$eCorresponding author
000137156 245__ $$aInflammation-induced alteration of astrocyte mitochondrial dynamics requires autophagy for mitochondrial network maintenance.
000137156 260__ $$aCambridge, Mass.$$bCell Press$$c2013
000137156 264_1 $$2Crossref$$3print$$bElsevier BV$$c2013-12-01
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000137156 520__ $$aAccumulating 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.
000137156 536__ $$0G:(DE-HGF)POF3-341$$a341 - Molecular Signaling (POF3-341)$$cPOF3-341$$fPOF III$$x0
000137156 542__ $$2Crossref$$i2013-12-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
000137156 542__ $$2Crossref$$i2014-12-03$$uhttps://www.elsevier.com/open-access/userlicense/1.0/
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000137156 650_7 $$2NLM Chemicals$$aAtg7 protein, mouse
000137156 650_7 $$2NLM Chemicals$$aCytokines
000137156 650_7 $$2NLM Chemicals$$aInterleukin-1beta
000137156 650_7 $$2NLM Chemicals$$aLipopolysaccharides
000137156 650_7 $$2NLM Chemicals$$aMicrotubule-Associated Proteins
000137156 650_7 $$2NLM Chemicals$$aReactive Oxygen Species
000137156 650_7 $$082115-62-6$$2NLM Chemicals$$aInterferon-gamma
000137156 650_7 $$0EC 1.14.13.39$$2NLM Chemicals$$aNitric Oxide Synthase Type II
000137156 650_7 $$0EC 3.6.5.5$$2NLM Chemicals$$aDnm1l protein, mouse
000137156 650_7 $$0EC 3.6.5.5$$2NLM Chemicals$$aDynamins
000137156 650_7 $$0EC 6.2.1.45$$2NLM Chemicals$$aAutophagy-Related Protein 7
000137156 650_2 $$2MeSH$$aAnimals
000137156 650_2 $$2MeSH$$aAstrocytes: cytology
000137156 650_2 $$2MeSH$$aAstrocytes: drug effects
000137156 650_2 $$2MeSH$$aAstrocytes: metabolism
000137156 650_2 $$2MeSH$$aAutophagy
000137156 650_2 $$2MeSH$$aAutophagy-Related Protein 7
000137156 650_2 $$2MeSH$$aCells, Cultured
000137156 650_2 $$2MeSH$$aCytokines: metabolism
000137156 650_2 $$2MeSH$$aDynamins: metabolism
000137156 650_2 $$2MeSH$$aInflammation: metabolism
000137156 650_2 $$2MeSH$$aInflammation: pathology
000137156 650_2 $$2MeSH$$aInterferon-gamma: pharmacology
000137156 650_2 $$2MeSH$$aInterleukin-1beta: metabolism
000137156 650_2 $$2MeSH$$aLipopolysaccharides: toxicity
000137156 650_2 $$2MeSH$$aMale
000137156 650_2 $$2MeSH$$aMice
000137156 650_2 $$2MeSH$$aMice, Inbred C57BL
000137156 650_2 $$2MeSH$$aMice, Transgenic
000137156 650_2 $$2MeSH$$aMicrotubule-Associated Proteins: genetics
000137156 650_2 $$2MeSH$$aMicrotubule-Associated Proteins: metabolism
000137156 650_2 $$2MeSH$$aMitochondria: drug effects
000137156 650_2 $$2MeSH$$aMitochondria: metabolism
000137156 650_2 $$2MeSH$$aMitochondrial Dynamics: drug effects
000137156 650_2 $$2MeSH$$aNitric Oxide Synthase Type II: metabolism
000137156 650_2 $$2MeSH$$aPhosphorylation
000137156 650_2 $$2MeSH$$aReactive Oxygen Species: metabolism
000137156 7001_ $$0P:(DE-HGF)0$$aPuyal, Julien$$b1
000137156 7001_ $$0P:(DE-HGF)0$$aToni, Nicolas$$b2
000137156 7001_ $$0P:(DE-HGF)0$$aGhanem, Alexander$$b3
000137156 7001_ $$0P:(DE-HGF)0$$aAngeloni, Cristina$$b4
000137156 7001_ $$0P:(DE-HGF)0$$aMalaguti, Marco$$b5
000137156 7001_ $$0P:(DE-HGF)0$$aCantelli-Forti, Giorgio$$b6
000137156 7001_ $$0P:(DE-HGF)0$$aBerninger, Benedikt$$b7
000137156 7001_ $$0P:(DE-HGF)0$$aConzelmann, Karl-Klaus$$b8
000137156 7001_ $$0P:(DE-HGF)0$$aGötz, Magdalena$$b9
000137156 7001_ $$0P:(DE-2719)9000369$$aWinklhofer, Konstanze F$$b10$$udzne
000137156 7001_ $$0P:(DE-HGF)0$$aHrelia, Silvana$$b11
000137156 7001_ $$0P:(DE-HGF)0$$aBergami, Matteo$$b12
000137156 77318 $$2Crossref$$3journal-article$$a10.1016/j.cmet.2013.11.005$$b : Elsevier BV, 2013-12-01$$n6$$p844-859$$tCell Metabolism$$v18$$x1550-4131$$y2013
000137156 773__ $$0PERI:(DE-600)2174469-5$$a10.1016/j.cmet.2013.11.005$$gVol. 18, no. 6, p. 844 - 859$$n6$$p844-859$$q18:6<844 - 859$$tCell metabolism$$v18$$x1550-4131$$y2013
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