| Project/Area Number |
08671599
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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 |
Cerebral neurosurgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
FUSE Takahisa Nagoya City University, Medical School, Instructor, 医学部, 助手 (00229080)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Taiji Nagoya City University, Medical School, Professor, 医学部, 教授 (60094364)
YAMADA Kazuo Nagoya City University, Medical School, Professor, 医学部, 教授 (90150341)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | p21 / p53 / Bax / glioma / heat stress / brain ischemia / HSP70 / stress response / p21 / p53 / ブリオーマ細胞 / HSP7c / サイクリン依存性キナーゼ インヒビター / 海馬錐体細胞 |
|---|
| Research Abstract |
The present study was designed to investigate the role of cyclin-dependent kinase (CDK) inhibitor p21 in several stress conditions.
Heat shock induces several events in cells including a series of gene expressions and cell cycle arrest. Recently several types of cell cycle arrest have been related to the function of CDK inhibitors. Here we show that heat shock treatment up-regulates p21 CDK inhibitor in A172 glioma cells and arrests the cell cycle at the G1 phase.
Next, we investigated the transient expression of p21 and p53 in rat brain after ischemia or subarachnoid hemorrhage.
Furthermore, in glioma cells, we found that heat treatment induced cell death in time and temperature-dependent manner. The nuclear staining with Hoechst33342 demonstrated morphological changes consistent with apoptosis. The TUNEL stain also demonstrated damages in the DNA.These morphological changes were accompanied by the accumulation of p53 and Bax. These results indicate that heat stress induced apoptosis in A172 glioma cells.
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