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Analysis of spatial and temporal protein expression in the cerebral cortex after ischemia-reperfusion injury.

Chen YH, Chiang YH, Ma HI - J Clin Neurol (2014)

Bottom Line: This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae.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.These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.

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.

No MeSH data available.


Related in: MedlinePlus

Silver staining of 2-D gels of cerebrocortical tissue in different regions, revealing some different protein expression patterns.
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Figure 2: Silver staining of 2-D gels of cerebrocortical tissue in different regions, revealing some different protein expression patterns.

Mentions: Two-dimensional gel electrophoresis maps were constructed for rat cortical proteins with or without tMCAO at pH 3-10. A typical 2-DE map of each group obtained from different cortical areas of the brain is shown in Fig. 2. After silver staining, about 400 spots in total were resolved in both maps and compared. There were no significant differences between the groups.


Analysis of spatial and temporal protein expression in the cerebral cortex after ischemia-reperfusion injury.

Chen YH, Chiang YH, Ma HI - J Clin Neurol (2014)

Silver staining of 2-D gels of cerebrocortical tissue in different regions, revealing some different protein expression patterns.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4017024&req=5

Figure 2: Silver staining of 2-D gels of cerebrocortical tissue in different regions, revealing some different protein expression patterns.
Mentions: Two-dimensional gel electrophoresis maps were constructed for rat cortical proteins with or without tMCAO at pH 3-10. A typical 2-DE map of each group obtained from different cortical areas of the brain is shown in Fig. 2. After silver staining, about 400 spots in total were resolved in both maps and compared. There were no significant differences between the groups.

Bottom Line: This study elucidated the mechanisms underlying ischemia-induced brain injury that results in neurological sequelae.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.These findings provide insights into the mechanisms underlying the neurodegenerative events that occur following cerebral ischemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurological Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.

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.

No MeSH data available.


Related in: MedlinePlus