| Project/Area Number |
23659631
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Hokkaido University |
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Principal Investigator |
OZAKI Michitaka 北海道大学, 大学院・保健科学研究院, 教授 (80256510)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | オートファジー / アポトーシス / p62/SQSTM1 / Nrf-2 / p62 / 細胞死 / 肝再生 |
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| Research Abstract |
In order to examine the regulatory role of autophagy and p62/SQSTM1 in fatty liver regeneration, we studied steatotic cell death (autophagy and apoptosis) in liver/hepatocytes.(1) Establishment of evaluation method for autophagy in cell/liver tissue. We tried to quantitatively evaluate autophagy of cells and liver tissue by expressions of LC3 and p62/SQSTM1, and electron micrograph.(2) We studied the regulatory mechanism of p62/SQSTM1 expression and its relation to apoptosis/autophagy and oxidative stress. p62/SQSTM1 expression was regulated by autophagy specifically, not by apoptosis, but also regulated positively by PI3-K/PDK/Akt-dependent signals. p62/SQSTM1 was also involved in suppression of cellular oxidative stress and injury. In mouse liver, p62/SQSTM1 increased cellular anti-oxidative molecules such as SOD, Ref-1 and Catalase through Nrf-2 and suppressed oxidative stress.
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