| Project/Area Number |
14207003
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Mie University |
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Principal Investigator |
TANAKA Toshio Mie University, Faculty of Medicine, Professor, 医学部, 教授 (00135443)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Yasuhito Mie University, Faculty of Medicine, Research Associate, 医学部, 助手 (40378427)
TSUNODA Hiroshi Nagoya University, University Hospital, Medical Doctor, 医学部附属病院, 医員 (20314114)
西村 有平 三重大学, 医学部, 講師 (30303720)
中 充子 三重大学, 医学部, 講師 (10093139)
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| Project Period (FY) |
2002 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥49,400,000 (Direct Cost: ¥38,000,000、Indirect Cost: ¥11,400,000)
Fiscal Year 2004: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
Fiscal Year 2003: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
Fiscal Year 2002: ¥35,620,000 (Direct Cost: ¥27,400,000、Indirect Cost: ¥8,220,000)
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| Keywords | vascular remodeling / proteome / stress protein / S100C / HSP72 / pulmonary hypertension / cerebral vasospasm / proteome database / 低酵素 / タウリン / クモ膜下出血 / 低酸素 / くも膜下出血 / トランスクリプトーム |
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| Research Abstract |
In this study, we have discovered that the stress protein system which induces in various diseases, and is guided becomes novel drug target and have elucidated the molecule mechanism. We exposed a focus to calcium-binding protein S100C which was the new hypoxia-induced gene which we have cloned originally and the other stress protein expression induction that we found newly and elucidated the pharmacoproteomic mechanism of vascular remodeling in various disease model. And I clarified proteome mechanism of pharmacoproteomic drug action by integration of the original pharmacoproteomic database and pharmacoproteomic experimental analysis. In pulmonary hypertension model by hypoxia treatment, we discovered that an expression induction of stress protein S100C through HIF-1 played an important role in remodeling of a pulmonary artery. (The PharmacogenomicsJ.3:183-188,2003). Furthermore, by metabolome analysis, the oral dosage of taurine suppressed the expression of S100C through HIF-1 and remodeling of a pulmonary artery and reported possibility as novel pulmonary hypertension therapeutics (The Pharmacogenomics J.3:183-188,2003). (Circulation. 110:1839-1846,2004). In addition, in a subarachnoid hemorrhage model, expression of stress protein HSP72 in cerebral basilar artery at the time of delayed cerebral basospasm, and the oral dosage of anti gastric ulcer medicine teprenone (Geranylgeranylacetone) induced an expression of stress protein HSP72 in a cerebral basilar artery more and discovered that I promoted improvement of cerebrovasospasm (Circulation. 110:1839-1846,2004). By these results of research, we elucidated novel pharmacoproteomic mechanisms of blood vessel remodeling. We have elucidation pharmacoproteomic mechanisms of stress protein induction in various disease model by pharmacoproteomic database and proteome analysis that we proposed ahead of the world in this study and this research strategy will be applied in more wide medical study in the near future.
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