O-linked β-N-acetylglucosamine modification of proteins is activated in post-ischemic brains of young but not aged mice: Implications for impaired functional recovery from ischemic stress.
Abstract
To evaluate the effect of age on the response of brains to an ischemic challenge,
we subjected young and aged mice to transient forebrain ischemia, and analyzed the
heat shock response and unfolded protein response, ubiquitin conjugation and SUMO
conjugation, and O-linked β-N-acetylglucosamine modification of proteins (O-GlcNAcylation).
The most prominent age-related difference was an inability of aged mice to activate
O-GlcNAcylation. Considering many reports on the protective role of O-GlcNAcylation
in various stress conditions including myocardial ischemia, this pathway could be
a promising target for therapeutic intervention to improve functional recovery of
aged patients following brain ischemia.
Type
Journal articleSubject
BrainAnimals
Mice, Inbred C57BL
Mice
Brain Ischemia
Myocardial Ischemia
Acetylglucosamine
SUMO-1 Protein
Psychomotor Performance
Recovery of Function
Protein Processing, Post-Translational
Aging
Male
Stroke
Ubiquitination
Stress, Physiological
Unfolded Protein Response
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https://hdl.handle.net/10161/23265Published Version (Please cite this version)
10.1177/0271678x15608393Publication Info
Liu, Shuai; Sheng, Huaxin; Yu, Zhui; Paschen, Wulf; & Yang, Wei (2016). O-linked β-N-acetylglucosamine modification of proteins is activated in post-ischemic
brains of young but not aged mice: Implications for impaired functional recovery from
ischemic stress. Journal of cerebral blood flow and metabolism : official journal of the International
Society of Cerebral Blood Flow and Metabolism, 36(2). pp. 393-398. 10.1177/0271678x15608393. Retrieved from https://hdl.handle.net/10161/23265.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Wulf Paschen
Professor in Anesthesiology
My research interests are understanding the mechanisms underlying induction of cell
death induced by a severe form of cellular stress. I am particularly interested in
the role of the endoplasmic reticulum in the pathological process induced by transient
cerebral ischemia and culminating in neuronal cell death. This pathological process
is associated with an irreversible suppression of protein synthese that limits the
ability of cells to withstand ischemia-induced impairment of endoplasmic r
Huaxin Sheng
Associate Professor in Anesthesiology
We have successfully developed various rodent models of brain and spinal cord injuries
in our lab, such as focal cerebral ischemia, global cerebral ischemia, head trauma,
subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord ischemia and compression
injury. We also established cardiac arrest and hemorrhagic shock models for studying
multiple organ dysfunction. Our current studies focus on two projects. One is to
examine the efficacy of catalytic antioxidant in treating cerebral is
Wei Yang
Associate Professor in Anesthesiology
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