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Autoren: van der Kooij, Michael A.
Rojas-Charry, Liliana
Givehchi, Maryam
Wolf, Christina
Bueno, Diones
Arndt, Sabine
Tenzer, Stefan
Mattioni, Lorenzo
Treccani, Giulia
Hasch, Annika
Schmeisser, Michael J.
Vianello, Caterina
Giacomello, Marta
Methner, Axel
Titel: Chronic social stress disrupts the intracellular redistribution of brain hexokinase 3 induced by shifts in peripheral glucose levels
Online-Publikationsdatum: 30-Jan-2023
Erscheinungsdatum: 2022
Sprache des Dokuments: Englisch
Zusammenfassung/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.
DDC-Sachgruppe: 610 Medizin
610 Medical sciences
Veröffentlichende Institution: Johannes Gutenberg-Universität Mainz
Organisationseinheit: FB 04 Medizin
Veröffentlichungsort: Mainz
Version: Published version
Publikationstyp: Zeitschriftenaufsatz
Nutzungsrechte: CC BY
Informationen zu den Nutzungsrechten:
Zeitschrift: Journal of molecular medicine
Seitenzahl oder Artikelnummer: 1441
Verlag: Springer
Verlagsort: Berlin u.a.
Erscheinungsdatum: 2022
ISSN: 1432-1440
DOI der Originalveröffentlichung: 10.1007/s00109-022-02235-x
Enthalten in den Sammlungen:DFG-491381577-H

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