scholarly journals Unraveling the ischemic brain transcriptome in a permanent middle cerebral artery occlusion mouse model by DNA microarray analysis

2011 ◽  
Vol 5 (2) ◽  
pp. 270-283 ◽  
Author(s):  
M. Hori ◽  
T. Nakamachi ◽  
R. Rakwal ◽  
J. Shibato ◽  
K. Nakamura ◽  
...  
Keyword(s):  
Mouse Model ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Microarray Analysis ◽  
Dna Microarray ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Ischemic Brain ◽  
Brain Transcriptome ◽  
Cerebral Artery Occlusion

scholarly journals Dendritic Cells Are Present in Ischemic Brain After Permanent Middle Cerebral Artery Occlusion in the Rat

Stroke ◽  
2002 ◽  
Vol 33 (4) ◽  
pp. 1129-1134 ◽  
Author(s):  
Nikolaos Kostulas ◽  
Hu-Lun Li ◽  
Bao-Guo Xiao ◽  
Yu-Min Huang ◽  
Vasilios Kostulas ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Ischemic Brain ◽  
Cerebral Artery Occlusion

Persistent Phosphorylation of Synaptic Proteins following Middle Cerebral Artery Occlusion

2002 ◽  
Vol 22 (9) ◽  
pp. 1107-1113 ◽  
Author(s):  
Shohei Matsumoto ◽  
Mehrdad Shamloo ◽  
Atsushi Isshiki ◽  
Tadeusz Wieloch
Keyword(s):  
Cell Signaling ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Brain Regions ◽  
Artery Occlusion ◽  
Ischemic Brain ◽  
Aberrant Cell ◽  
Synaptosomal Fraction ◽  
Cerebral Artery Occlusion

Transient cerebral ischemia following 1 to 2 hours of middle cerebral artery occlusion (MCAO) in the rat leads to infarction, which can be diminished by synaptic transmission modulators, implying aberrant cell signaling in the pathogenetic process. The authors report here changes in the levels of tyrosine phosphorylated proteins (PTyr) and calcium calmodulin kinase II (CaMKII) phosphorylation of Thr 286, in synaptosomal, particulate, and cytosolic fractions of different cortical areas following 1 or 2 hours of MCAO, or 2 hours of MCAO followed by 2 hours of reperfusion. At the end of 2-hour MCAO, PTyr, and in particular the pp180, indicative of NR2A/B subunit, increased in the synaptosomal fraction in less ischemic areas while it decreased in more severe ischemic regions. During reperfusion, phosphorylation increased at least 2-fold in all reperfused areas. During 2 hours of MCAO, the phosphorylation of CaMKII increased 8- to 10-fold in the synaptosomal fraction in all ischemic brain regions. During reperfusion, the phospho-CaMKII levels remained elevated by approximately 300% compared with the contralateral hemisphere (control). There was no increase in phospho-CaMKII in the cytosolic fraction at any time during or following ischemia in any of the brain regions examined. The authors conclude that both tyrosine kinase coupled pathways, as well as CaMKII-mediated cellular processes associated with synaptic activity, are strongly activated during and particularly following MCAO. These results support the hypothesis that aberrant cell signaling may contribute to ischemic cell death and dysfunction, and that selective modulators of cell signaling may be targets for pharmacological intervention against ischemic brain damage.

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