| Project/Area Number |
26460338
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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 |
General pharmacology
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| Research Institution | Kyoto University |
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Principal Investigator |
MINAMI Manabu 京都大学, 医学研究科, 講師 (90511907)
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| Co-Investigator(Renkei-kenkyūsha) |
SENO Hiroshi 京都大学, 大学院医学研究科, 教授 (90335266)
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| Research Collaborator |
NAKATSUJI Masato
YASUI Mika
FUJIKAWA Risako
HIGUCHI Sei
FUKUMITSU Ryu
IKEDO Taichi
NAGATA Manabu
HAYASHI Kosuke
MIYATA Takeshi
YANG Tao
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | EPRAP / マクロファージ / 慢性炎症 / シグナル情報伝達 / 翻訳後修飾 / シグナル情報伝達系 |
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| Outline of Final Research Achievements |
EP4 receptor-associated protein, EPRAP, has been identified as a novel cytoplasmic regulator of macrophage activation, which inhibits MEK-ERK pathway activation induced by inflammatory stimuli. In this study, we aimed to dissect the significance and pathophysiological roles of EPRAP on chronic inflammation in vivo. We generated EPRAP-deficient mice as well as transgenic mice with enforced expression of EPRAP in macrophages, and created various animal models of chronic inflammatory diseases. Our study demonstrated that EPRAP deficiency markedly worsened the inflammatory phenotypes and outcomes of inflammatory bowel disease and pulmonary fibrosis. Our results indicated that EPRAP plays crucial roles in the pathogenesis of chronic inflammatory diseases; and EP4-EPRAP signaling could be a novel diagnostic or therapeutic target for refractory chronic diseases.
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