Involvement of ER stress pathway in chronic inflammatory diseases.
| 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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Report
(5 results)
Research Products
(12 results)
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[Journal Article] Increased oxidative stress impairs adipose tissue function in sphingomyeline synthase I null mice.2013
Author(s)
M. Yano, T. Yamamoto, N. Nishimuras, T. Gotoh, K. Watanabe, K. Ikeda, Y. Garan, R. Taguchi, K. Node, T. Okazaki, Y. Oike.
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Journal Title
Related Report
Peer Reviewed
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[Journal Article] Tunicamycin inhibits diabetes.2012
Author(s)
N. Shaabani, N. Honke, P.A. Lang, B. Gorg, P. Proksch, N. Gailus, T. Gotoh, D. Haussinger, K.S. Lang.
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Journal Title
Cell Physiol. Biochem.
Volume: 29
Issue: 3-4
Pages: 595-602
DOI
Related Report
Peer Reviewed
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[Journal Article] Deletion of C/EBP homologous protein (Chop) in C57Bl/6 mice dissociates obesity from insulin resistance.2012
Author(s)
M. Maris, L. Overbergh, C. Gysemans, A. Waget, A.K. Cardozo, E. Verdrengh, J.P. Cunha, T. Gotoh, M. Cnop, D.L. Eizirik, R. Burcelin, C. Mathieu.
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Journal Title
Diabetologia
Volume: 55
Issue: 4
Pages: 1167-1178
DOI
Related Report
Peer Reviewed
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