| Project/Area Number |
07557230
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 試験 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
MURANO Shunichi Chiba Univ.of Medicine Assistant, 医学部, 助手 (50231634)
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| Co-Investigator(Kenkyū-buntansha) |
KOMUKAI Masayuki Toubishi Yakuhin Co., Oume Laboratory., 青梅研究所, 研究員
MORISAKI Nobuhiro Chiba Univ.of Medicine Lecturer, 医学部, 講師 (40174411)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1996: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | Vascular smooth muscle cell / Profilin / migration / unstable plaque / actin binding protein / gene therapy / antisense / 平滑筋細胞 / 動脈硬化 / ballooning / Boyden chamber / リポソーム法 |
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| Research Abstract |
Migration of vascular smooth muscle cells from the medial to the intimal membrane is important in initiation and development of atherosclerosis. Therefore we can possibly prevent the initiation and development of atherosclerosis through a control of the migration. Actin-binding proteins are closely involved in migration of smooth muscle cells. For example one of the proteins, calponin, was reported to inhibit the migration of smooth muscle cells and consequently to prevent the progress of experimental atherosclerosis. Profilin is one of the major actin-binding proteins and is suspected to play an inportant role in cell movement. In this project, we assessed if profilin could be a target of gene therapy by which we can prevent the progress of atherosclerosis through regulation of the smooth muscle cell migration. First we cloned a human profilin gene from a cDNA library of human skeletal muscle cells. We inserted the cDNA into an expression vector and transfected it into cultured vascular smooth muscle cells. Finally migration was rather accelerated by the transfection of profilin gene. But the experiment was done only under a condition of trangent expression. The result must be confirmed by cells with permanent expression of profilin gene. Additionally, we developed a new model of atherosclerosis to use it in in vivo experiments of this project. The model has a unique atherosclerotic plaque (an unstable plaque). The pathology of the plaque is quite similar to that of clinically risky human atherosclerosis. The model is very useful to assess the effects of various interventions including the profilin gene therapy.
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