2017 Fiscal Year Final Research Report
Treatment for acute pancreatitis by regulating autophagy which modulates zymogen granules and inflammasomes
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 |
Research Field |
Gastroenterology
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Research Institution | Osaka University |
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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Keywords | 急性膵炎 / オートファジー |
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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Free Research Field |
消化器内科学
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