MECHANISMS OF ACUTE VASCULAR REACTION TO INJURY

急性血管损伤反应的机制

• 批准号: 3097360
• 负责人: EARL P BENDITT
• 金额: $ 100.16万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-03-01 至 1988-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3097360
• 关键词: atherosclerosis; hypertension; vascular endothelium; vascular smooth muscle

This program has a common interest in responses of large and small vessels and of their endothelial and smooth muscle cells to injury. Fundamental questions are being asked related to basic pathologic processes that may be involved in atherosclerosis. Mechanisms that permit or stimulate cell replication, cell migration and cellular interactions are being investigated. The potential role of mechanical and toxic injuries, of the metabolic products of xenobiotics and the mechanism whereby herpesviruses may produce proliferative lesions in animals and human beings are being investigated. The program includes studies of the nature of changes in ploidy of smooth muscle with age and hypertension studies. Mechanisms of interaction of leukocytes, endothelial cells, of the HDL apoprotein and ApoSAA are also being investigated. A wide range of methods are being used including cell culture, histoimmunocytochemistry, flow cytophotometry, scanning electron microscopy and molecular probes for viral and amyloid genes in cells.

本程序对大型和小型船舶的响应有共同的兴趣 以及它们的内皮细胞和平滑肌细胞的损伤。基本原理 正在询问与基本病理过程有关的问题，这些过程可能 与动脉粥样硬化有关。允许或刺激细胞的机制 复制、细胞迁移和细胞相互作用正在 调查过了。机械和中毒损伤的潜在作用， 外源生物的代谢产物和疱疹病毒的作用机制 可能会在动物和人类身上产生增殖性损伤 调查过了。该计划包括对变化的性质的研究 血管的倍性与年龄和高血压的研究。机制： 高密度脂蛋白载脂蛋白与白细胞、内皮细胞的相互作用 ApoSAA也在接受调查。 目前正在使用一系列方法，包括细胞培养， 组织免疫细胞化学、流式细胞术、扫描电子显微镜 以及细胞中病毒和淀粉样蛋白基因的分子探针。