| Project/Area Number |
08457062
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Kyushu University |
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Principal Investigator |
SUEISHI Katsuo Kyushu University, Faculty of Medicine, Professor, 医学部, 教授 (70108710)
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| Co-Investigator(Kenkyū-buntansha) |
TASHIRO Yoshihiko Kyushu University, Faculty of Medicine, Assistant, 医学部, 助手 (10188237)
HASHIMOTO Shuichi Kyushu University, Faculty of Medicine, Assistant, 医学部, 助手 (00243931)
KONO Shinji Kyushu University, School of Health Science, Assistant Professor, 医療技術短期大学部, 助教授 (20225379)
NAKAGAWA Kazunori Kyushu University, Faculty of Medicine, Assistant, 医学部, 助手 (50217668)
NAKASHIMA Yutaka Kyushu University, Faculty of Medicine, Assistant, Professor, 医学部, 助教授 (50135349)
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| Project Period (FY) |
1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1996: ¥6,700,000 (Direct Cost: ¥6,700,000)
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| Keywords | gene therapy / HVJ-lipsome method / VEGF / p53 / atherosclerosis / angiogenesis / apoptosis / NO |
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| Research Abstract |
1. Vascular remodeling and intimal neovascularization : 1) The density of intimal angiogenesis in human corrnary arteries was well correlated to the atherosclerotic luminal stenosis, and its activity represented one of histological characteristics of atherosclerotic progression, 2) VEGF expressed by smooth muscle cells and macrophages participated in this angiogenic process. 3) VEGF gene transfer by the HVJ-liposome method induced angiomatoid proliferation in fibrocellularly thickened intima of rabbit carotid arteries.
2. Biological characteristics of gene transfer method with HVJ-liposomes : The transfer efficiency and cytotoxic effects of this method was estimated in vascular wall, hepatic sinusoids, respiratory system and cancer cells.
3. Wild-type p53 gene transfer was highly effective to suppress the intimal thickening following balloon injury.
4. Chronic suppression of vascular NO synthesis with L-NAME induced myocardial arteriosclerosis probably via the activation of renin-angiotensis system within vascular wall.
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