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Research on mechanism for localization of atherosis by micromechanical analysis of vascular endothelial cell

血管内皮细胞微力学分析定位动脉粥样硬化机制

基本信息

批准号：
12480270
负责人：
TSUJIOKA Katsuhiko
金额：
$ 8.9万
依托单位：
Kawasaki Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2002
项目状态：
已结题

项目摘要

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 sequentiallyAfter 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 processWe conclude that vascular endothelial cell becomes permissive state for monocyte to invade into space under endothelial cell, and monocyte moves quickly after attachment

虽然血液和血压的含量在身体的各个部分中仅显示出微小的差异，但病理学研究表明动脉粥样硬化斑块局限于动脉的弯曲或分叉处，因此局部血流状况作为动脉粥样硬化发生和发展的局部化机制而受到关注。作为动脉粥样硬化形成的初始过程，推测单核细胞侵入血管内皮细胞下的空间，成为巨噬细胞，摄取氧化的LDL，从而形成动脉粥样硬化斑块。然而，关于单核细胞与血管内皮细胞之间的相互作用，特别是机械相互作用的研究却很少。本文分析了内皮细胞的运动和粘弹性。此外，我们还检测了内皮细胞内应力纤维和粘着斑激酶的变化。最后，我们观察了单核细胞如何三维有序地侵入内皮细胞下的空间。单核细胞附着在内皮细胞上后，内皮细胞与基质的距离增加，而细胞与细胞的距离没有变化。单核细胞的粘附降低了内皮细胞的弹性。单核细胞的粘附减少了内皮细胞内的应力纤维和粘着斑激酶。单核细胞贴壁后立即开始向内皮细胞下方移动，30分钟后移动过程趋于稳定。说明血管内皮细胞已进入允许单核细胞侵入内皮细胞下方的状态，贴壁后单核细胞移动速度较快

项目成果

期刊论文数量（54）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Noriyuki Kataoka, Kanso Iwaki, Ken Hashimoto, Seiichi Mochizuki, Yasuo Ogasawara, Masaaki Sato, Katsuhiko Tsujioka, and Fumihiko Kajiya: "Measurements of endothelial cell-to-cell and cell-to-substrate gaps and micromechanical properties of endothelial cel

Noriyuki Kataoka、Kanso Iwaki、Ken Hashimoto、Seiichi Mochizuki、Yasuo Ogasawara、Masaaki Sato、Katsuhiko Tsujioka 和 Fumihiko Kajiya：“内皮细胞间和细胞间间隙的测量以及内皮细胞的微机械特性