Analysis of Spatial and Temporal Protein Expression in the Cerebral Cortex after Ischemia-Reperfusion Injury
Journal of Clinical Neurology
;
: 84-93, 2014.
Article
in English
| WPRIM
| ID: wpr-84617
ABSTRACT
BACKGROUND AND PURPOSE:
Hypoxia, or ischemia, is a common cause of neurological deficits in the elderly. This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae.METHODS:
Cerebral ischemia was induced in male Sprague-Dawley rats by transient ligation of the left carotid artery followed by 60 min of hypoxia. A two-dimensional differential proteome analysis was performed using matrix-assisted laser desorption ionization-time-of-flight mass spectrometry to compare changes in protein expression on the lesioned side of the cortex relative to that on the contralateral side at 0, 6, and 24 h after ischemia.RESULTS:
The expressions of the following five proteins were up-regulated in the ipsilateral cortex at 24 h after ischemia-reperfusion injury compared to the contralateral (i.e., control) side aconitase 2, neurotensin-related peptide, hypothetical protein XP-212759, 60-kDa heat-shock protein, and aldolase A. The expression of one protein, dynamin-1, was up-regulated only at the 6-h time point. The level of 78-kDa glucose-regulated protein precursor on the lesioned side of the cerebral cortex was found to be high initially, but then down-regulated by 24 h after the induction of ischemia-reperfusion injury. The expressions of several metabolic enzymes and translational factors were also perturbed soon after brain ischemia.CONCLUSIONS:
These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Mass Spectrometry
/
Aconitate Hydratase
/
Brain Injuries
/
Carotid Arteries
/
Reperfusion Injury
/
Cerebral Cortex
/
Brain Ischemia
/
Rats, Sprague-Dawley
/
Proteome
/
Dynamin I
Limits:
Aged
/
Humans
/
Male
Language:
English
Journal:
Journal of Clinical Neurology
Year:
2014
Type:
Article
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