| Project/Area Number |
09671266
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | First Department of Surgery, Hyogo College of Medicine |
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Principal Investigator |
NAKAI Yoshiyuki Hyogo College of Medicine, First Department of Surgery, , assistant professor, 医学部, 講師 (50198024)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMA Tomoko Hyogo College of Medicine, Department of Genetics, associated Professor, 医学部, 助教授 (10172868)
TAKEUCHI Masaharu Hyogo College of Medicine, First Department of Surgery, assistant professor, 医学部, 助手 (00258162)
FUJIMOTO Jiro Hyogo College of Medicine, First Department of Surgery, assistant professor, 医学部, 講師 (90199373)
TOYOSAKA Akihiro Hyogo College of Medicine, First Department of Surgery, Professor, 医学部, 助教授 (20068498)
OKAMOTO Eizo Hyogo College of Medicine, First Department of Surgery, Professor, 医学部, 教授 (50068425)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Liver Cirrhosis / Portal hypertension / Hepatocyte growth factor / Gene therapy / Vascular endothelial growth factor / hemagglutinating virus of Japan / VEGF / 門脈圧亢進症ラットモデル / 肝硬変ラットモデル |
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| Research Abstract |
Liver cirrhosis is the irreversible end result of fibrous scarring. The competent therapy has not been established now. We have studied the gene therapy for liver cirrhosis. To treat liver cirrhosis rats, we established a simple and safe in vivo fransfection procedure of repeatedly transducing skeletal muscles with the human HGF gene using liposomes containing the hemagglutinating virus of Japan. In rats injected repeatedly with HGF-HVJ liposome, transfection of the human HGF gene increased the production of endogenous rat HGF in vivo and suppressed the increase of the transforming growth factor and fibrosis in both the periportal and centrilobular liver diminished and deformation of the liver acinus decreased. In the meantime, liver cirrhosis made portal hypertension, which had a development of collateral veins. We also studied the relalionship between the development of collateral veins and vascular endothelial growth factor (VEGF), In the liver and small intesline of portal hypertensive rats, immunochemical study and western blotting confirmed the expression of VEGF, but the receptor of VEGF was not detected in the endothelial cels of collateral veins. Therefore, the relationship between angiogeneisis of collateral vein and VEGF was not proved.
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