| Project/Area Number |
26860255
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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 |
Experimental pathology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
Ooshio Takako 旭川医科大学, 医学部, 助教 (80723238)
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| Co-Investigator(Renkei-kenkyūsha) |
NISHIKAWA Yuji 旭川医科大学, 医学部, 教授 (90208166)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | JNK / MKK7 / 肝細胞増殖 / 肝修復 / 肝再生 / 肝臓 / 細胞増殖 / 細胞運動 / 病理学 / 肝傷害 / 肝線維化 |
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| Outline of Final Research Achievements |
The MKK7 which is an upstream regulator of JNKs is suggested to be involved liver proliferation and regeneration, but roles of MKK7 in liver pathophysiology remain obscure. Here we examined the effects of hepatocyte-specific MKK7 knockout (KO) on liver regeneration and repair processes. After a single injection of CCl4, reparation of the injured liver was delayed in KO mice, despite the extent of liver injury and robust regenerative proliferation of hepatocytes that were comparable to control. In hepatocytic spheroids in collagen gel culture (CGC), MKK7 KO suppressed branching morphogenesis and reduced the expression of transgelin and plasminogen activators. Overexpressed these genes in cultured MKK7 KO hepatocytes rescued the attenuated branching morphogenesis in CGC. Our study demonstrates that hepatic MKK7 has important roles in repair processes following liver injury, possibly through promoting migration and morphogenesis of hepatocytes.
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