| Project/Area Number |
24659364
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Osaka University |
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Principal Investigator |
TAKEHARA Tetsuo 大阪大学, 医学(系)研究科(研究院), 教授 (70335355)
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| Co-Investigator(Kenkyū-buntansha) |
TATSUMI Tomohide 大阪大学, 大学院医学系研究科, 助教 (20397699)
HIKITA Hayato 大阪大学, 大学院医学系研究科, 寄附講座 助教 (20623044)
SHIGEKAWA Minoru 大阪大学, 大学院医学系研究科, 医員 (00625436)
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| Co-Investigator(Renkei-kenkyūsha) |
IKEZAWA Kenji 大阪大学, 大学院医学系研究科, 大学院生
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 急性膵炎 / アポトーシス / マウスモデル / 膵炎 / STAT3 / Bcl-xL / ノックアウトマウス |
|---|
| Research Abstract |
STAT3 is a transcription factor which controls several gene expression levels associated with cell proliferation, inflammation, and cell survival. In the study, we clarified STAT3 played a protective role in pancreatic necrosis, inflammatory cell infiltration and apoptotic cell death using caerulein-administrated conditional STAT3 knockout mice, In the models of caerulein or L-arginine-induced acute pancreatitis, while the expression levels of Bcl-xL and Mcl-1 (anti-apoptotic proteins) increased, the severity of pancreatitis did not worsen in conditional Bcl-xL knockout mice compared with control mice. Collectively, these results suggested that Bcl-xL and Mcl-1may function redundantly in regulation of acute pancreatitis.
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