| Project/Area Number |
10670840
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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 |
Radiation science
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| Research Institution | Fukui Medical University |
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Principal Investigator |
MATUMOTO Hideki Fukui Medical University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (40142377)
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHI Sachiko Fukui Medical University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (00218570)
KANO Eiichi Fukui Medical University, Faculty of Medicine, Professor, 医学部, 教授 (70065910)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2000: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Glioma / p53 / Inducible nitric oxide synthase / Hsp72 / Intracellular signal transduction / Intercellular signal transduction / Radiosensitivity / Bystander effect / ヒト舌扁平上皮癌細胞 / X-rays / Inducible Nitric Oxide Synthase / Nitric Oxide / Conditioned Medium |
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| Research Abstract |
Nitric oxide(NO)is known to be a multi-functional physiological substance. Recently, nitric oxide is suggested to be involved in p53-dependent response to many kinds of stress such as heat shock, ionizing radiation and changes in cellular metabolism. To verify this hypothesis we examined the effect of nitric oxide produced endogenously by heat-shocked or irradiated cells on non-stressed cells using human glioblastoma cells and squamous cell carcinoma cells bearing either wild-type or mutant p53 gene. Nitric oxide excreted from the treated donor cells with heat-shock or radiation could modulate thermo-or radiosensitivity of recipient cells through induction of intracellular signal transduction. Our finding of the accumulation of p53 and hsp72 in NO-recipient cells co-cultivated with treated NO-donor cells provides the first evidence for an intercellular signal transduction pathway via NO as an intermediate without cell-to-cell interactions such as gap junctions. It is suggested that NO is one of factors for bystander effect induced by environmental stress such as heat-shock or radiation. Collectively, these findings indicate the importance of an intercellular signal transduction pathway intiated by nitric oxide in the cellular response to heat-shock or ionizing radiation on hyperthermia or radiotherapy of cancer.
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