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，细胞凋亡在细胞凋亡的形成中起作用。 动脉粥样硬化病变和最终狭窄的血管， 病变进展。具体目标侧重于 半胱氨酸蛋白酶和Fas/FasL途径在控制细胞死亡中的作用 血管平滑肌这包括在动物中使用半胱天冬酶抑制剂 死亡被认为在其中起着关键作用的模型， 一只转基因小鼠在一个决定死亡的共同瓶颈处被阻断， 通过Fas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， 包括两项体外和体内研究，以探索 纤维蛋白凝胶收缩作为血管狭窄的机制。最后， 将研究选定的人和小鼠动脉粥样硬化组织， 根据体外鉴定的分子确定模型的相关性 或在动物模型中。