SMOOTH MUSCLE CELL APOPTOSIS

平滑肌细胞凋亡

• 批准号: 6575709
• 负责人: Stephen MARK Schwartz
• 金额: $ 6.54万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-03-01 至 2003-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6575709
• 关键词: CD95 molecule; apoptosis; atherosclerotic plaque; cell adhesion; cell growth regulation; cysteine endopeptidases; fibrin; gene expression; human tissue; laboratory mouse; laboratory rabbit; laboratory rat; protein purification; protein structure function; tissue /cell culture; vascular smooth muscle; wound healing

Project 1 proposes that apoptosis plays a role in the formation of atherosclerotic lesions and in the ultimate narrowing of the vessel as lesions progress. The Specific Aims focus on the possible role of the cystein proteases and the Fas/FasL pathway in controlling cell death in vascular smooth muscle. This includes use of caspase inhibitors in animal models in which death has been thought to play a key role, and development of a transgenic mouse blocked at a common choke point determining death mediated via Fas and related receptors. These studies will include exploration of the role of death in controlling intramural coagulation, including two studies in vitro and in vivo to explore the possible role of fibrin gel contraction as a mechanism of vascular narrowing. Finally, selected human and mouse atherosclerotic tissues will be studied to determine the relevance of models based on molecules identified in vitro or in animal models.

项目1提出凋亡在形成中起作用 动脉粥样硬化病变和船只的最终狭窄 病变进展。具体目的侧重于 Cystein蛋白酶和FAS/FASL途径控制细胞死亡 血管平滑肌。这包括在动物中使用caspase抑制剂 人们认为死亡起着关键作用和发展的模型 在确定死亡的公共扼流点阻塞的转基因小鼠的 通过FA和相关受体介导。这些研究将包括 探索死亡在控制壁内凝血中的作用， 包括两项体外研究和体内研究，以探讨 纤维蛋白凝胶收缩是血管变窄的机制。最后， 将研究选定的人和小鼠动脉粥样硬化组织 确定基于体外鉴定的分子的模型的相关性 或在动物模型中。