| Project/Area Number |
24790741
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
ISAGAWA Takayuki 東京医科歯科大学, 難治疾患研究所, 助教 (40418637)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | macrophage / inflammation / NFkB / metabolism / マクロファージ / 炎症終息 / NFKB / 代謝 |
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| Research Abstract |
It is well known that chronic inflammation forms the basis of cancers and the metabolic syndrome. Therefore, in the present study, we performed a comprehensive, genome-wide examination of the targets of NFkBs, the central transcriptional regulator of inflammation, in the context of regulatory mechanisms of inflammation in macrophages. As a result, we revealed that NFkB subunit switching occurs during the transition from the inflammatory response phase to the resolution phase. Furthermore, we found that p50, a NFkB subunit, regulates inflammatory genes during the early inflammatory phase but then shifts to regulating metabolic genes during the resolution phase. We also revealed that p50 is involved in the metabolic reprogramming associated with the inflammatory response.
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