Gutenberg Open Science: Chronic social stress disrupts the intracellular redistribution of brain hexokinase 3 induced by shifts in peripheral glucose levels

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-8295

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DC Field	Value	Language
dc.contributor.author	van der Kooij, Michael A.	-
dc.contributor.author	Rojas-Charry, Liliana	-
dc.contributor.author	Givehchi, Maryam	-
dc.contributor.author	Wolf, Christina	-
dc.contributor.author	Bueno, Diones	-
dc.contributor.author	Arndt, Sabine	-
dc.contributor.author	Tenzer, Stefan	-
dc.contributor.author	Mattioni, Lorenzo	-
dc.contributor.author	Treccani, Giulia	-
dc.contributor.author	Hasch, Annika	-
dc.contributor.author	Schmeisser, Michael J.	-
dc.contributor.author	Vianello, Caterina	-
dc.contributor.author	Giacomello, Marta	-
dc.contributor.author	Methner, Axel	-
dc.date.accessioned	2023-01-30T08:52:52Z	-
dc.date.available	2023-01-30T08:52:52Z	-
dc.date.issued	2022	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/8311	-
dc.description.abstract	Chronic stress has the potential to impair health and may increase the vulnerability for psychiatric disorders. Emerging evidence suggests that specific neurometabolic dysfunctions play a role herein. In mice, chronic social defeat (CSD) stress reduces cerebral glucose uptake despite hyperglycemia. We hypothesized that this metabolic decoupling would be reflected by changes in contact sites between mitochondria and the endoplasmic reticulum, important intracellular nutrient sensors, and signaling hubs. We thus analyzed the proteome of their biochemical counterparts, mitochondria-associated membranes (MAMs) from whole brain tissue obtained from CSD and control mice. This revealed a lack of the glucose-metabolizing enzyme hexokinase 3 (HK3) in MAMs from CSD mice. In controls, HK3 protein abundance in MAMs and also in striatal synaptosomes correlated positively with peripheral blood glucose levels, but this connection was lost in CSD. We conclude that the ability of HK3 to traffic to sites of need, such as MAMs or synapses, is abolished upon CSD and surmise that this contributes to a cellular dysfunction instigated by chronic stress.	en_GB
dc.description.sponsorship	Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 491381577	de
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	Chronic social stress disrupts the intracellular redistribution of brain hexokinase 3 induced by shifts in peripheral glucose levels	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-8295	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 04 Medizin	de
jgu.organisation.number	2700	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	Journal of molecular medicine	de
jgu.journal.volume	100	de
jgu.pages.start	1441	de
jgu.pages.end	1453	de
jgu.publisher.year	2022	-
jgu.publisher.name	Springer	de
jgu.publisher.place	Berlin u.a.	de
jgu.publisher.issn	1432-1440	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	610	de
jgu.publisher.doi	10.1007/s00109-022-02235-x	de
jgu.organisation.ror	https://ror.org/023b0x485	-
jgu.subject.dfg	Lebenswissenschaften	de
Appears in collections:	DFG-491381577-H

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