| Project/Area Number |
23590365
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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 |
Pathological medical chemistry
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| Research Institution | Kumamoto University |
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Principal Investigator |
GOTOH TOMOMI 熊本大学, 教育学部, 教授 (20264286)
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| Co-Investigator(Renkei-kenkyūsha) |
OIKE Yuichi 熊本大学, 大学院生命科学研究部, 教授 (90312321)
ENDO Motoyoshi 熊本大学, 大学院生命科学研究部, 助教 (40398243)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 小胞体 / 細胞小器官 / ストレス応答 / アポトーシス / ミトコンドリア / 虚血再灌流障害 / 細胞内ストレス応答 / 細胞内小器官 / 細胞酸素消費速度 / 小胞体ストレス / ゴルジ体 / 活性酸素 / CHOP / ミトコンドリアストレス / 炎症 |
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| Outline of Final Research Achievements |
We previously reported that ER stress-CHOP pathway is involved in the formation of atherosclerosis, especially in plaque instability. In this study, we clarified that ER stress-CHOP pathway is involved in the myocardial re-perfusion injury. In this model, we also showed that oxygen radical is involved in the activation of ER stress-CHOP pathway. Treatment with oxygen radical scavenger rescued re-perfusion injury. We also showed that damage of cartilage tissue in OA is mediated by ER stress pathway. Next, we clarified that abnormality of lipid species in ER-Golgi-cell membrane compartment influences mitochondrial function, using SMS1-knock out mice. Recently, it is reported that each organelle stress influence other organelle functions. Therefore, we analyzed a novel putative mitochondrial molecule to clarify the influences on ER in mitochondrial stress. We clarify that putative mitochondrial diseases-related molecule TMEM65 is a mitochondrial inner-membrane protein.
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