| Project/Area Number |
18590944
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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 | The University of Tokushima |
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Principal Investigator |
MITSUI Takao The University of Tokushima, University Medical and Dental Hospital, Assistant Professor (80294726)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Yukiko University Medical and Dental Hospital, Insittute of Health Biosciences, Graduate School, Assistant member of schcol affairs (70398014)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,870,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | glucocorticoid / mitochondria / transcription / グリココルチコイド |
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| Research Abstract |
We found that production of the reaction oxygen species (ROS) was related to the mitochondrial dysfunctional in the skeletal muscle with a long term glucocorticoid treatment. Furthermore, because it was thought that the effect was direct action for mitochondria by the glucocorticoid, it was drawn up to clarify these points in this study more, and an interesting result was provided. We analyzed the effect of corticosteroid on the mitochondria membrane potential (ΔΨm), generation of ROS and influence of the apoptosis in various kinds of cultured cells. In the differentiated cells, the dexamethasone addition let ROS generation and apoptosis increase with a fall of ΔΨm. These changes were not seen under the existence of SOD. In the proliferating cells, the dexamethasone let ROS generation and apoptosis increase with increase of ΔΨm. The ROS production and the increase of the apoptosis disappeared under the existence of SOD, but the increase of ΔΨm did not change. These results suggested that activated glucocorticoid receptors were moved to the mitochondria in these cells. Furthermore, these indicated the existence of protein to guide to the mitochondria although it had been well recognized that the activated glucocorticoid acceptor shifted in a nucleus. We introduced the GFP protein of the glucocorticoid acceptor into cultured cell (COS, RD) to examine whether an activated glucocorticoid acceptor shifted to mitochondria under dexamethasone treatment (1 x 10^<6-> x 10^<-7>M). GFP signals were observed in the mitochondria in addition to nuclei. This strongly suggested the existence of the protein which carried a glucocorticoid acceptor to mitochondria.
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