Toll-like receptor 4 mediates lung ischemia-reperfusion injury
| Project/Area Number |
21591811
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | Mie University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAO Motoshi 三重大学, 医学部附属病院, 准教授 (30263007)
SHOMURA Shin 三重大学, 医学部附属病院, 医員 (70452224)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 外科 / 移植・再生医療 / シグナル伝達 |
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| Research Abstract |
Ischemic preconditioning is mediated a MyD88-independent pathway, leading to NF-κB activation and protection against lung ischemia reperfusion injury. We conclude that an activation of MyD88 or TRIF, which are associate proteins of Toll-like receptor 4, would regulate a role of NF-κB to injure or preserve lung function.
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Report
(4 results)
Research Products
(7 results)
