| Project/Area Number |
24591125
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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 |
Respiratory organ internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOHYAMA Tadashi 帝京大学, 医学部, 教授 (00302703)
城 大祐 東京大学, 学内共同利用施設等, 助教 (30376470)
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| Co-Investigator(Renkei-kenkyūsha) |
JO Taisuke 東京大学, 保健健康推進本部, 保健センター助教 (30376470)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 上皮間葉転換 / LIGHT/TNFSF14 / E-cadherin / Vimentin / LIGHT/ TNFSF14 / EMT |
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| Outline of Final Research Achievements |
LIGHT/TNFSF14 has been reported to be up-regulated in airway inflammation in severe asthma and has been recognized to be related to the pathogenesis of severe asthma. LIGHT enhanced TGF-b-induced epithelial mesenchymal transition in vitro, and further LIGHT itself induced epithelial mesenchymal transition in human airway epithelial cells through Erk1/2 pathway. LIGHT would be associated with the pathogenesis of airway remodeling.
In addition, LIGHT induced several cytokines and chemokines from human bronchial epithelia cells, some of which are suggested to be important in the pathogenesis of severe asthma. LIGHT/TNSFS14 would be suggested to be one of the candidates for the molecular target therapy for inflammatory airway diseases, including severe asthma.
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