1996 Fiscal Year Final Research Report Summary
Stress Response in Cerebral Ischemia and the Role of Ubiquitin
| Project/Area Number |
07457305
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | University of Tokyo |
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Principal Investigator |
KIRINO Takaaki University of Tokyo, Faculty of Medicine, Department of Neurosurgery, Proferror, 医学部・附属病院, 教授 (90126045)
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| Co-Investigator(Kenkyū-buntansha) |
IDE Takafumi University of Tokyo, Faculty of Medicine, Department of Neurosurgery, Assistant, 医学部・附属病院, 助手 (40262000)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Cerebral ischemia / Ubiquitin / Stress protein / Stress response / Cell death / Hippocampus / Mongolian gerbil / Immunostaining |
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| Research Abstract |
Cerebral ischemia is one of the most frequent metabolic stress to the brain. A brief period of ischemia does not kill neurons and it triggers stress response. Once stress proteins are induced, neurons acquire transient tolerance to further ischemia. Ubiquitin is one of such stress proteins. In CA1 pyramidal cells, however, free ubiquitin is depleted far before delayd neuronal death following ischemia. Our experiment has shown this by immunostaining, immunoblotting, immunoprecipitation, and immunoabsorption assays. By ELISA quantitation, we also have shown the depletion of free form of ubiq and concomitant increase in conjugated ubiquitin in CA1 neurons following ischemia. In-situ hybridization method using c-DNA complimentary to gerbil ubiquitin gene, gene expression for ubiquitin is rather enhanced following ischemia. This transient increase in transcription yet decrease in translation is also seen in hsp 70 gene following ischemia. The mechanism of delayd neuronal death of CA1 neurons is still unknown. Although the actual role of ubiquitin in neuronal death is also not known, further investigation of ubiquitin gene expression might reveal the mechanism of this form of neuronal in hippocampal Ca1 neurons.
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