Interaction between the autophagy protein Beclin 1 and Na+,K+-ATPase during starvation, exercise, and ischemia.

Details

Serval ID
serval:BIB_AB89E0F43EE9
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Interaction between the autophagy protein Beclin 1 and Na+,K+-ATPase during starvation, exercise, and ischemia.
Journal
JCI insight
Author(s)
Fernández Á.F., Liu Y., Ginet V., Shi M., Nah J., Zou Z., Zhou A., Posner B.A., Xiao G., Tanguy M., Paradis V., Sadoshima J., Rautou P.E., Puyal J., Hu M.C., Levine B.
ISSN
2379-3708 (Electronic)
ISSN-L
2379-3708
Publication state
Published
Issued date
16/01/2020
Peer-reviewed
Oui
Volume
5
Number
1
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Autosis is a distinct form of cell death that requires both autophagy genes and the Na+,K+-ATPase pump. However, the relationship between the autophagy machinery and Na+,K+-ATPase is unknown. We explored the hypothesis that Na+,K+-ATPase interacts with the autophagy protein Beclin 1 during stress and autosis-inducing conditions. Starvation increased the Beclin 1/Na+,K+-ATPase interaction in cultured cells, and this was blocked by cardiac glycosides, inhibitors of Na+,K+-ATPase. Increases in Beclin 1/Na+,K+-ATPase interaction were also observed in tissues from starved mice, livers of patients with anorexia nervosa, brains of neonatal rats subjected to cerebral hypoxia-ischemia (HI), and kidneys of mice subjected to renal ischemia/reperfusion injury (IRI). Cardiac glycosides blocked the increased Beclin 1/Na+,K+-ATPase interaction during cerebral HI injury and renal IRI. In the mouse renal IRI model, cardiac glycosides reduced numbers of autotic cells in the kidney and improved clinical outcome. Moreover, blockade of endogenous cardiac glycosides increased Beclin 1/Na+,K+-ATPase interaction and autotic cell death in mouse hearts during exercise. Thus, Beclin 1/Na+,K+-ATPase interaction is increased in stress conditions, and cardiac glycosides decrease this interaction and autosis in both pathophysiological and physiological settings. This crosstalk between cellular machinery that generates and consumes energy during stress may represent a fundamental homeostatic mechanism.
Keywords
Autophagy, Cell Biology, Cell stress
Pubmed
Web of science
Create date
21/01/2020 9:33
Last modification date
02/04/2020 6:19
Usage data