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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

Typical appearance of infarct areas in the rat brain at 24 h after transient occlusion of the middle cerebral artery. Normal tissues are stained purple with 2,3,5-triphenyltetrazolium chloride; infarcted tissue remains unstained. The appearance of this tissue relative to the sham-operated controls (data not shown) was similar to that of the nonlesioned contralateral hemispheres. The percentage volume of the hemispheric true infarct was typically 18-22%.
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Figure 1: Typical appearance of infarct areas in the rat brain at 24 h after transient occlusion of the middle cerebral artery. Normal tissues are stained purple with 2,3,5-triphenyltetrazolium chloride; infarcted tissue remains unstained. The appearance of this tissue relative to the sham-operated controls (data not shown) was similar to that of the nonlesioned contralateral hemispheres. The percentage volume of the hemispheric true infarct was typically 18-22%.

Mentions: The true infarct volume obtained 24 h after tMCAO was 306.17 mm3 (n=3). Infarcted tissues were found predominantly on the lesioned sides of the cortices (Fig. 1). No infarctions were observed on the nonlesioned sides or in the sham-operated controls.


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)

Typical appearance of infarct areas in the rat brain at 24 h after transient occlusion of the middle cerebral artery. Normal tissues are stained purple with 2,3,5-triphenyltetrazolium chloride; infarcted tissue remains unstained. The appearance of this tissue relative to the sham-operated controls (data not shown) was similar to that of the nonlesioned contralateral hemispheres. The percentage volume of the hemispheric true infarct was typically 18-22%.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Typical appearance of infarct areas in the rat brain at 24 h after transient occlusion of the middle cerebral artery. Normal tissues are stained purple with 2,3,5-triphenyltetrazolium chloride; infarcted tissue remains unstained. The appearance of this tissue relative to the sham-operated controls (data not shown) was similar to that of the nonlesioned contralateral hemispheres. The percentage volume of the hemispheric true infarct was typically 18-22%.
Mentions: The true infarct volume obtained 24 h after tMCAO was 306.17 mm3 (n=3). Infarcted tissues were found predominantly on the lesioned sides of the cortices (Fig. 1). No infarctions were observed on the nonlesioned sides or in the sham-operated controls.

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