Journal article
Effects of pharmacological inhibition of AMP-activated protein kinase on GLUT3 expression and the development of ischemic tolerance in astrocytes
Neuroscience research, Vol.84, pp.68-71
07/2014
DOI: 10.1016/j.neures.2014.04.007
PMID: 24815515
Abstract
•We examine the effects of AMPK inhibition during sublethal preconditioning ischemia.•AMPK inhibition suppresses GLUT3 at the end of ischemia.•The inhibition enhances GLUT3 expression during reperfusion.•Increased GLUT3 expression induces more glycogen synthesis during reperfusion.•AMPK-GLUT3 contributes to the development of astrocytic ischemic tolerance.
Ischemic tolerance resulting from preconditioning ischemia is a neuroprotective mechanism. In cultured astrocytes, its development depends on regulation of the expression of glucose transporter 3 (GLUT3) by the stress sensor/effector AMP-activated protein kinase (AMPK). Here we demonstrate that GLUT3 is upregulated during preconditioning and then downregulated during recovery. We also found that, although AMPK inhibition during preconditioning initially suppressed the upregulation of GLUT3 as shown previously, this was followed by a period of GLUT3 upregulation, enhanced glycogen accumulation, and enhanced tolerance to a subsequent ischemic challenge. These results reveal that AMPK has a complex influence on ischemic tolerance.
Details
- Title: Subtitle
- Effects of pharmacological inhibition of AMP-activated protein kinase on GLUT3 expression and the development of ischemic tolerance in astrocytes
- Creators
- Sadahiro Iwabuchi - Department of Molecular Physiology & Biophysics, University of Iowa Carver College of Medicine, Iowa City, USAKoichi Kawahara - Laboratory of Cellular Cybernetics, Graduate School of Information Science and Technology, Hokkaido University, Sapporo, JapanN. Charles Harata - Department of Molecular Physiology & Biophysics, University of Iowa Carver College of Medicine, Iowa City, USA
- Resource Type
- Journal article
- Publication Details
- Neuroscience research, Vol.84, pp.68-71
- Publisher
- Elsevier Ireland Ltd
- DOI
- 10.1016/j.neures.2014.04.007
- PMID
- 24815515
- ISSN
- 0168-0102
- eISSN
- 1872-8111
- Grant note
- DOI: 10.13039/501100001691, name: Japan Society for the Promotion of Science; DOI: 10.13039/100000968, name: American Heart Association; DOI: 10.13039/100001595, name: Dystonia Medical Research Foundation; DOI: 10.13039/100006152, name: Edward Mallinckrodt, Jr. Foundation; DOI: 10.13039/100000001, name: National Science Foundation; DOI: 10.13039/100001391, name: Whitehall Foundation
- Language
- English
- Date published
- 07/2014
- Academic Unit
- Molecular Physiology and Biophysics
- Record Identifier
- 9984025575202771
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