| Project/Area Number |
25460863
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Uemura koichi 東京医科歯科大学, 医歯(薬)学総合研究科, 教授 (30244586)
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| Co-Investigator(Kenkyū-buntansha) |
AKI TOSHIHIKO 東京医科歯科大学, 大学院医歯学総合研究科, 講師 (60304474)
FUNAKOSHI TAKESHI 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (40444715)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ユビキチン-プロテアソーム系 / ヒ素 / 心筋 / アポトーシス / ユビキチンプロテアソーム系 / Parkin / ユビキチン－プロテアソーム系 / 亜ヒ酸 / 心筋由来細胞 / apoptosis / ubiquitin-proteasome系 |
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| Outline of Final Research Achievements |
Although arsenic is poison, it is used for a treatment of acute promyelocytic leukemia with a secondary effect of cardiac toxicity, e.g. fatal arrythmia. To elucidate the mechanisms of arsenic on heart we studied the toxicity of arsenic trioxide on mice atrial muscle-derived HL-1 cells. We applied 1-10μM ATO for 24h and studied the characterization of cell death, the effects of ubiquitin ligase Parkin, the change of ubiquitin-proteasome syastem and autophagy-lysosome system. The result is that ATO activate Parkin and ubiquitin-proteasome system in cardiac HL-1 cells, and, induces quality control of mitochondria and maintenance of cell homeostasis, thereby, cell protection.
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