| Project/Area Number |
17591321
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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 | The University of Tokyo |
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Principal Investigator |
SHIGEMATSU Kunihiro The University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部附属病院, 助手 (20215966)
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| Co-Investigator(Kenkyū-buntansha) |
MIYATA Tesuro The University of Tokyo, Faculty of Medicine, Associate Professor, 医学部附属病院, 助教授 (70190791)
DEGUCHI Jyun-o The University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部附属病院, 助手 (80323591)
KIMURA Hideo The University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部附属病院, 助手 (60327070)
NISHIKAGE Seiji The University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部附属病院, 助手 (30431844)
岡本 宏之 東京大学, 医学部附属病院, 助手 (60348266)
石井 誠之 東京大学, 医学部附属病院, 助手 (80365197)
重松 宏 東京大学, 医学部附属病院, 助教授 (40134556)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Surgery / Signal pathway / transplant / regenerative medicine / Vascular / Cell / Tissue |
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| Research Abstract |
The common carotid artery of white rabbits was injured by the passage of 2F Forgaty catheter (x3). The injured carotid artery with thickened intima was replaced with ePTFE graft with 2mm diameter 28days after injury. However, the thickened intima was dissected by clamping procedures and the replaced grafts were riot always found to be patent. In addition to the dissection, diameter difference between the prosthesis and the injured host artery with thickened intima was one of the reasons of occlusion of the replaced grafts. Therefore, we changed the protocol, and the graft replacement was performed in the rabbits of which carotid artery was injured 1 or 2 weeks before. At first, we studied the differences of ERK and PKB activity and the expression of cyclin D1 at the time point 1 and 2 weeks after injury as the Vor control in the replacement model. The activities of ERK and PKB at the time point 1 and 2 weeks after injury was amost similar to that of uninjured artery. However, cyclin D1 expression was higher 1 and 2 weeks after injury than that of uninjured artery. These showed that smooth muscle cells in thickened intima 1 and 2 weeks after injury were in the cell cycle of growth. And then, we studied the ERK, PKB, and cyclin D1 expression in the intima SMC of prosthesis at the time point of 1 and 2 weeks after graft replacement. ERK and PKB of intima were not impressively activated compared to those of 2 weeks after balloon injury. And cycline D1 expression was higher, but not significant, than that of 2 weeks after balloon injury. These results may show the possibilities that the anastomotic intimal hyperplasia could be controlled by blocking the signal pathway via ERK and PKB activitivation.
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