2013 Fiscal Year Final Research Report
Molecular mechanisms of acinar cell injury in acute pancreatitis
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 |
Research Field |
Gastroenterology
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Research Institution | Osaka University |
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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Keywords | 急性膵炎 / アポトーシス / マウスモデル |
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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[Journal Article] Pancreatic STAT3 protects mice against caerulein-induced pancreatitis via PAP1 induction2012
Author(s)
Shigekawa M, Hikita H, Kodama T, Shimizu S, Li W, Uemura A, Miyagi T, Hosui A, Kanto T, Hiramatsu N, Tatsumi T, Takeda K, Akira S, Takehara T.
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Journal Title
Am J Pathol
Volume: 101
Pages: 2105-2113
Peer Reviewed
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