| Project/Area Number |
15K10551
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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 |
Anesthesiology
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| Research Institution | The Tazuke Kofukai |
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Principal Investigator |
ADACHI Takehiko 公益財団法人田附興風会, 医学研究所 第9研究部, 部長 (90252428)
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| Co-Investigator(Kenkyū-buntansha) |
広田 喜一 関西医科大学, 医学部, 教授 (00283606)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 酸素環境 / 敗血症 / 急性肺障害 / thioredoxin / TXNIP / HIF-1 / 低酸素誘導性因子1 / 急性肺傷害 |
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| Outline of Final Research Achievements |
The aim of this study is to evaluate the clinical significance of the cellular redox system consisting of thioredoxin and thioredoxin interacting protein (Txnip) for the protection against inflammatory disorders including septi shock, ALI, and ARDS. Since inflammation has been associated with hypoxia and the resulting dysregulation of oxygen homeostasis, we investigated the functional interaction between the thioredoxin system and hypoxia-inducible factor 1 (HIF-1) under inflammatory conditions. We showed that thioredoxin enhanced the transcriptional activity of HIF-1. Thioredoxin-induced HIF-1 activation up-regulated the expression level of Txnip, which could, in turn, suppress the function of thioredoxin. These results revealed that the cellular redox environment was maintained by a subtle balance and interplay between these redox-related molecules.
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