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Molecular Pathological Study on Endothelial Regulation of Blood-Vascular Wall Interaction

内皮调节血管壁相互作用的分子病理学研究

基本信息

批准号：
04454180
负责人：
SUEISHI Katsuo
金额：
$ 4.61万
依托单位：
Kyushu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

项目摘要

The Interaction between blood and vascular wall is dynamic and endothelial cells play a centralrole in the regulation of its interaction and the maintenance of vascular function. In this projectwe investigated the role of endothelial function in the development of thrombosis, atherosclerosis and angiogenesis. The main results obtained in this project are as follows.1. Endothelial function in thrombogenesis : In rabbits with Shwartzman reaction, 1)tissue factor(TF) was immunohistochemically expressed by not only Kupffer cells but endothelial cells, 2)this expression of TF seemed to be partly regulated by the expression of IL-1 beta ra by Kupffer cells, 3)the TF expression by endothelial cells was noted at abluminal side as well as luminal surface. Inaddition, the localization of TF mRNA was also observed by in situ hybridization using human TF cDNAprobes.2. Regulation mechanism of angiogenesis : We clarified that the angiogenic induction was enhanced by hypoxia, which stimulated glial cells and cancer cells to release VEGF and bFGF.Re-oxigenation of hypoxic endothelials also up-regulated the receptors for VEGF and bFGF on the endothelial surface.3. Endothelial function in the atherosclerotic progression : In the patients with inflammatory abdominal aortic aneurysm, which generally follows abdominal aortic atherosclerosis, IE genome of human cytomegalovirus wad strongly expressed by endothelial cells of vasa vasora as well as macrophages and fibroblast-like mesen-chamal cells and seemed to participate essentially in the progression of its inflammatory process.

血液与血管壁之间的相互作用是动态的，内皮细胞在调节其相互作用和维持血管功能中起着核心作用.本课题研究了内皮功能在血栓形成、动脉粥样硬化和血管生成中的作用。本项目取得的主要成果如下：1.内皮细胞在血栓形成中的作用：在Shwartzman反应兔中，1）Kupffer细胞和内皮细胞均表达组织因子（TF），2）Kupffer细胞表达IL-1 β ra可能部分调节TF的表达，3）内皮细胞表达TF的部位不仅限于管腔表面，还包括近腔侧。此外，采用人TF cDNA探针进行原位杂交，观察TF mRNA的定位.血管生成的调控机制：阐明了缺氧可促进血管生成，刺激胶质细胞和癌细胞释放VEGF和bFGF，缺氧内皮细胞再氧化也可上调内皮细胞表面VEGF和bFGF受体.动脉粥样硬化进展中的内皮功能：在腹主动脉粥样硬化后的炎性腹主动脉瘤患者中，血管内皮细胞、巨噬细胞和成纤维细胞样间质细胞强烈表达人巨细胞病毒IE基因组，并可能参与其炎症过程。