| Project/Area Number |
12480270
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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 |
Biomedical engineering/Biological material science
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
TSUJIOKA Katsuhiko Kawasaki Medical School, Dep. Medicine Professor, 医学部, 教授 (30163801)
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| Co-Investigator(Kenkyū-buntansha) |
MOCHIZUKI Seiichi Kawasaki College of Allied Health Professions, Div. Clinical Engineer, Assistant Professor, 臨床工学科, 助教授 (60259596)
KAJIYA Fumihiko Okayama University, Graduate School of Medicine and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (70029114)
OGASAWARA Yasuo Kawasaki Medical School, Dep. Medicine Assistant Professor, 医学部, 助教授 (10152365)
IWAKI Kanso Hayashibara Biochemical Laboratories, Inc, Fujisaki Institute, Subdirector, 藤崎研究所, サブディレクター(研究職)
KATAOKA Noriyuki Kawasaki College of Allied Health Professions, Div. Clinical Engineer, Lecturer, 臨床工学科, 講師 (20250681)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥13,900,000 (Direct Cost: ¥13,900,000)
Fiscal Year 2002: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2001: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2000: ¥4,900,000 (Direct Cost: ¥4,900,000)
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| Keywords | vascular endothelial cell / monocyte / atherosclerosis / micromechanics / atomic force microscope / ECIS / マイクロメカニス / 原子間分顕微鏡 / マイクロメカニクス |
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| Research Abstract |
Although the content of blood and blood pressure show only small difference in every portion in the body, pathological study revealed that atherosclerotic plague is localized at curvature or bifurcation of artery, and thus local blood flow condition has been given attention as a mechanism for localozation of initiation and progression of athrosclerosis. As an initial process of atherogenosis, it has been speculated that monocyte invades into space under vascular endothelial cell, and becomes macrophage to take oxidized LDL and thus form atherosclerotic plague. However, only little is revealed about interaction especially mechanical interaction between monocyte and vascular endothelial cell. In this study we analyzed the movement and viscoelastic property of endothelial cell. In addition, we examined the change of stress fiber and focal adhesion kinase within endothelial cell. Finally we observed how monocyte invades into space under endothelial cell three-dimensionaly and sequentially
After attachment of monocyte on the endothelial cell, the distance between endothelial cell and substrate increased, but cell to cell distance did no change. The elasticity of endothelial cell was decreased by the attachment of monocyte. The attachment of monocyte decreased stress fiber and focal adhesion kinase within endothelial cell. The monocyte began to move into space under endothelial cell immediately after attachment onto endothelial cell and after 30 minutes movement became steady process
We conclude that vascular endothelial cell becomes permissive state for monocyte to invade into space under endothelial cell, and monocyte moves quickly after attachment
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