2003 Fiscal Year Final Research Report Summary
Molecular mechanism of Onset of Acute Pancreatily in Pancreatic Acinar Cells
| Project/Area Number |
14570450
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Jichi Medical School |
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Principal Investigator |
OHNISHI Hirohide Jichi Medical School, Dept.of Gastroentery, Assistant Professor, 医学部, 講師 (00313023)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Pancreatitis / Syntoxin / vacuolation / Pancreatic cell / 空胞形成 |
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| Research Abstract |
Although the precise molecular mechanism of the onset of acute pancreatitisis is still unclear, the intracellular vacuolation formed by the heterotopic fusion of lysozomes and zymogen granules is assumed to be the pathogenic early event in the acute pancreatitis. To elucidate the molecular mechanism of the pathological vacuolation, we conducted this study to investigate the involvement SNARE proteins in the abnormal vacuolation using the model system of intracellular vacuolation formed by cytotoxin VacA (J.Olin.Invest. 107 : 363-370, 2001). We have elucidated that syntaxin 7, a member of SNARE family, is involved in the pathological intracellular vacuolation (J.Biol.Chem. 278 : 25585-25590, 2003). We extended our study to elucidate the molecular mechanism of pancreatic fibrosis, which results from acute pancreatitis, using isolated pancreatic stellate cells. We have shown that acvitin A, a member of TGF-β family, is an autocrine activator of pancreatic stellate cells. We have further revealed that TGF-β family activates pancreatic stellate cells and promotes their growth through distinct Smads-dependent pathways.
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