Cell-type-specific role of STAT3 in non-alcoholic steathepatitis
Project/Area Number |
22790631
|
Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Gastroenterology
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Research Institution | Gunma University |
Principal Investigator |
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 非アルコール性脂肪性肝炎 / STAT3 / メチオニンコリン欠乏食 / 細胞特異 / 細胞特異性 / SREBP1 / NASH / 炎症細胞 / IL-10 / MCD食 / 高脂肪食 / 非アルコール性脂肪性肝炎(NASH) / 脂質沈着 / SREBP1c / ノックアウトマウス |
Research Abstract |
The cell type specific role of STAT3 was examined by using hepatocyte-specific STAT3 knockout mice and macrophage/neutrophil specific STAT3 knockout mice. Both knockout mice and control wild type mice were fed with methionine-choline deficient diet, which is a murine NASH model. We have shown activation of STAT3 in hepatocyte prevents steatosis by inhibiting SREBP1c activation. On the other hand, we have revealed activation of STAT3 in macrophage/neutrophil accelerates inflammation in the liver, while it prevents steatosis by STAT3 activation in hepatocytes.
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Report
(4 results)
Research Products
(36 results)