| Project/Area Number |
24590991
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
ITOH Yoshito 京都府立医科大学, 医学(系)研究科(研究院), 教授 (70244613)
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| Co-Investigator(Renkei-kenkyūsha) |
藤田 潤 京都大学, 医学研究科, 教授 (50173430)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 脂肪肝炎 / 肝細胞癌 / Apg-2 / 熱ショック蛋白 / APG-2 / 部分肝切除 / 肝細胞がん / 肝炎 |
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| Outline of Final Research Achievements |
Expression level of Apg-2, which is one of the Hsp110 family members and reported to be overexpressed in human hepatocellular carcinomas, was upregulated in hepatocytes in high fat diet (HFD)-induced mouse fatty liver models. However, HFD-induced liver steatosis, obesity and lipid accumulation in adipose tissues were greatly ameliorated in Apg-2 KO mouse. Furthermore, to examine the role of Apg-2 in hepatocarcinogenesis, we used DEN-induced models and found that both the incidence and tumor size of hepatocellular carcinomas were significantly decreased in Apg-2 KO mouse. Consequently, these results suggest that Apg-2 plays important roles in liver steatosis and hepatocarcinogenesis through their chaperoning activities.
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