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Delayed genomic responses to transient middle cerebral artery occlusion in the rat

Title
Delayed genomic responses to transient middle cerebral artery occlusion in the rat
Authors
Kim J.-B.Piao C.-S.Lee K.W.Han P.-L.Ahn J.I.Lee Y.S.Lee J.-K.
Ewha Authors
한평림
SCOPUS Author ID
한평림scopus
Issue Date
2004
Journal Title
Journal of Neurochemistry
ISSN
0022-3042JCR Link
Citation
Journal of Neurochemistry vol. 89, no. 5, pp. 1271 - 1282
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Ischemic stress in the brain induces acute and massive neuronal death in the targeted area, which is followed by a second round of detrimental processes, called delayed neuronal death, in the neighboring areas. To test the hypothesis that transcriptional control plays a role in the pathophysiology of the postischemic brain, the genomic responses that occurred in the brain at 3, 6 and, 12 h, and 1, 2 or 4 days after transient middle cerebral artery occlusion (MCAO) were examined using a microarray harboring 5000 rat cDNAs. This analysis indicated that the number of up-regulated genes was gradually increased, along with the concomitant reduction in the number of down-regulated genes, until 12 h to 1 day after MCAO. It was followed by a delayed surge of down-regulated genes at 2 days after MCAO. Northern blots and immunohistological analysis confirmed the validity of these microarray data. We present a list of 85 genes that were up-regulated more than 2.3-fold between 12 h and 4 days after MCAO, which included 56 novel genes whose expression has not previously been implicated in ischemic pathophysiology. The list included genes involved in oxidative stress, inflammation, extracellular matrix (ECM), neuronal development and differentiation processes. Together these results suggest that the pathophysiology of the postischemic brain proceeds by the transcriptional activation of genes related to the process of delayed neuronal damage and/or recovery and repair.
DOI
10.1111/j.1471-4159.2004.02429.x
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일반대학원 > 뇌·인지과학과 > Journal papers
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