1998 Fiscal Year Final Research Report Summary
Experimental analysis of therapeutic windows in cerebral ischemia
| Project/Area Number |
08670725
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Keio University |
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Principal Investigator |
TANAKA Kortaro Keio University, Department of Neurology, Associate Professor, 医学部, 専任講師 (90129528)
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| Co-Investigator(Kenkyū-buntansha) |
NAGATA Eiichiro Keio University, Department of Neurology, Instructor, 医学部, 助手 (00255457)
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| Project Period (FY) |
1996 – 1998
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| Keywords | Cerebral ischemia / Cerebral infarction / Therapeutic window / cyclic AMP / Signal transduction / Protein kinase / Penumbra |
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| Research Abstract |
Phosphorylation of cyclic AMP response element binding protein (CREB) is one of the most important mechanisms controlling various gene transcriptions. In the present study, the phosphorylation of CREB was examined immunohistochemically at 24 hours of recirculation following 1.5 hours of middle cerebral artery occlusion (MCAO) in rats. MCAO was induced by the intraluminal suture method. The infarct core revealed a significant reduction in the number of immunoreactive cells with the anti-phosphorylated CREB and with the anti-CREB antibody, which binds to both unphosphorylated and phosphorylated CREB.In contrast, the pen-infarct area exhibited a marked increase in the number of immunopositive cells as well as in the intensity of nuclear staining with each antibody, so that almost all of the cells expressing CREB demonstrated phosphorylation of CREB.On the other hand, about half of the CREB immunopositive cells reacted weakly with the anti-phosphorylated CREB antibody in the sham group. These findings indicated that the expression as well as phosphorylation of CREB protein was significantly activated in the regions surrounding the infarct area. Since phosphorylation of CREB has recently been implicated in signal transductions that promote the survival and differentiation of neurons, the present data suggest that tissue repair mechanisms may be markedly activated in the pen-infarct area.
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