| Project/Area Number |
10480249
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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 Physiology, Kawasaki Medical School, Professor, 医学部, 教授 (30163801)
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| Co-Investigator(Kenkyū-buntansha) |
OGASAWARA Yasuo Medical Engineering, Kawasaki Medical School, Assistant Professor, 医学部, 助教授 (10152365)
KAJIYA Fumihiko Medical Engineering, Kawasaki Medical School, Professor, 医学部, 教授 (70029114)
OCHI Kazunori Physiology, Kawasaki Medical School, Research Assistant, 医学部, 助手 (50069077)
IWAKI Kanzo Hayasibara Biochemical Laboratories, inc., Researcher, 藤崎研究所, 副主事
MOCHIZUKI Seiichi Medical Engineering, Kawasaki College of Allied Health Professions, Assistant Professor, 臨床工学科, 助教授 (60259596)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 1999: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1998: ¥10,400,000 (Direct Cost: ¥10,400,000)
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| Keywords | Atherosclerosis / Local Blood Flow / Endotherial Cell / Monocyte / Adhension Molecule / Nitric Oxide Synthase / 細胞動態 / 局所血流 / 内皮細胞 / 細胞接着因子 / NO合成酵素 |
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| Research Abstract |
Although there are many studies by using molecular biology of receptor, lipid metabolism and pathological analysis to analyze the initiation and evolution of atherosclerosis, there are only few studies about the mechanism of localization of atherosclerosis. As one of the characteristic features of atherosclerosis is its localization to curvature or bifurcation of artery, recently many researchers pay attention to the local blood flow structure as an initiator of atherosclerosis. In this study we focused on the function of vascular endothelial cell and interaction of endothelial cell and monocyte, and analyzed the initial process, which leads the localization of atherosclerosis. The endothelial nitric oxide synthase (eNOS) was stained with fluorescent labeled antibody, and nitric oxide (NO) production was visualized fluorescence material DAF2. The eNOS expression and NO production was reduced and heterogeneous at the bifurcation of renal artery from aorta, where atherosclerosis is prone
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to occur. On the other hand, the expression of cell adhesion molecule was increased at the atherosclerosis-prone area. NO prevents adhesion of platelets and suppress the growth of vascular smooth muscle, and thus inhibits the initiation of atherosclerosis. We analyzed the effect of adhesion of monocyte to endothelial cell motion by the electric cell-substrate impedance sensing system (ECIS). Within one hour after monocyte adhesion to interleukin stimulated endothelial cell, the impedance decreased substantially. This decrease of impedance is mainly due to the increase off cell to substrate space, not to the increase of cell to cell space. We conclude that the local blood flow condition may initiate atherosclerosis via the decrease of NO production due to the decreased expression of eNOS and the increase of monocyte adhesion due to the increase of the expression of adhesion molecule. The monocyte loosens the attachment of endothelial cell to the substrate via the signal transduction system. Less
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