| Project/Area Number |
16K15429
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
巽 智秀 大阪大学, 医学系研究科, 講師 (20397699)
疋田 隼人 大阪大学, 医学系研究科, 助教 (20623044)
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| Research Collaborator |
IWAHASHI Kiyoshi 大阪大学, 大学院医学系研究科
SUEYOSHI Hironari 大阪大学, 大学院医学系研究科
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 急性膵炎 / オートファジー |
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| Outline of Final Research Achievements |
We examined the change of acinar cell autophagy in acute pancreatitis and its impact on progression of the disease. By analyzing autophagy-related proteins in mice with caerulein-induced acute pancreatitis, autophagy was suggested to be promoted with decrease in Rubicon expression. To examine the impact of autophagy inhibition on caerulein-induced acute pancreatitis, we generated pancreas-specific Atg7 knock out mice. However, they developed temporary acute pancreatitis followed by chronic pancreatitis with severe atrophic change without any stimulation. Therefore, we next successfully generated tamoxifen-inducible acinor cell-specific Atg7 Knock out mice. We confirmed that tamoxifen injection into them suppressed Atg7 expression in their pancreas.
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