Pin1 is decreased in ischemically damaged liver and suppressed liver regeneration after hepatectomy through the inhibition of Pin1-mediated NF-kappaB activation in hepatocytes.
| Project/Area Number |
23791516
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Chiba University |
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Principal Investigator |
KUBOKI Satoshi 千葉大学, 医学部附属病院, 助教 (50571410)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 肝臓外科学 / 術後肝再生 |
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| Research Abstract |
Pin1 was degraded in severe damaged liver, therefore, regeneration was suppressed through decreased activation of NF-kappaB. In contrast, Pin1 expression was maintained in mild damaged liver. Therefore, Pin1 bound to NF-kappaB-p65 and generated Pin1-NF-kappaB-p65 complex. This complex activated NF-kappaB and induced liver regeneration. Moreover, cell proliferation was inhibited in severe damaged hepatocyte induced by H2O2 stimulation in vitro, through decreased expression of Pin1 and Pin1-NF-kappaB-p65 complex and decreased activation of NF-kappaB. In conclusion, Pin1 is an important endogenous regulator of liver regeneration in severe damaged liver,and is a potential therapeutic target for liver failure after extended hepatectomy.
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Report
(3 results)
Research Products
(13 results)
