| Project/Area Number |
20590777
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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 | Osaka University |
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Principal Investigator |
HIRAMATSU Naoki (2009-2010) Osaka University, 医学系研究科, 講師 (30362700)
松本 仁 (2008) Osaka University, 医学系研究科, 助教 (80467505)
|
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| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Hitoshi 大阪大学, 医学系研究科, 助教 (80467505)
MIYOSHI Eiji 大阪大学, 医学系研究科, 教授 (20322183)
平松 直樹 大阪大学, 医学系研究科, 助教 (30362700)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 肝臓学 / 糖鎖 / 脂肪肝 / GnT-V / NASH / MCP-1 / ERストレス / 小胞体ストレス / メタボリックシンドローム |
|---|
| Research Abstract |
N-Acetylglucosaminyltransferase V (GnT-V), catalyzing beta1-6 branching in asparagine-linked oligosaccharides, is known to promote cancer metastasis, and its expression is increased in chronic hepatitis (CH) progression. Using GnT-V transgenic (Tg) mice, we found GnT-V prevented hepatic inflammation and fibrosis in a mouse CH model through modulation of lymphocyte and HSC function. Moreover, we also found GnT-V prevented hepatocyte cholesterol accumulation which led to ameliorate hepatocyte sensitivity to inflammation. These results indicated expression of GnT-V in CH would prevent disease progression as a self-defense reaction.
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