| Project/Area Number |
15K19354
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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 |
Gastroenterology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
Yuichi Kojima 大阪医科大学, 医学部, 助教 (10747744)
|
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| Research Collaborator |
Nakagawa Takatoshi
Harada Satoshi
Asahi Michio
Higuchi Kazuhide
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ERストレス / オートファジー / NSAIDｓ誘引性小腸潰瘍 / 小腸障害 / NSAIDs |
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| Outline of Final Research Achievements |
Our aim was to discover a novel therapeutic molecular target for NSAIDs-induced intestinal ulcer. To achieve this, we explored how ER stress response, autophagy, and apoptosis were mutually interacted in the onset and development of the disorder. During a period of this grant, our colleagues reported that NSAIDs-induced intestinal ulcer was mitigated in intestine-specific autophagy-deficient mice, and a collagen loss caused by the fascinated turnover contributed to the onset of the disorder. Subsequently, we revealed that the fascinated turnover of collagen was caused by an E3 ligase, pVHL, which was published in peer-reviewed journal. Consequently, we could our research in review article in 2017. In addition, we published several clinical reports in regard to maximizing the established pharmacological therapy by using a state of art endoscopic investigation.
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