MECHANISM FOR CARDIOPROTECTION IN HSF1 KNOCKOUT MICE

HSF1 敲除小鼠的心脏保护机制

• 批准号: 6121198
• 负责人: IVOR BENJAMIN
• 金额: $ 0.82万
• 依托单位: UT SOUTHWESTERN MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-09-15 至 1999-08-14
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6121198
• 关键词: Mammalia; animal tissue; biomedical resource; cardiovascular system; genetically modified animals; nuclear magnetic resonance spectroscopy; technology /technique

The broad, long-term goal of this project is to elucidate the mechanisms by which specific stress proteins reduce oxidative damage, and to develop strategies by which the heat shock family of stress proteins can increase ischemic cardioprotection. One of the specific aims is to establish whether gain of function of specific stress protein expression, under the control of an inducible-system, will rescue ischemic susceptibility of HSF1-deficient mice through effects that ameliorate oxidative stress/damage, enhance cardiac metabolism, and restore ventricular function. We have initiated studies to assess cardiac metabolism and function using (1) both the Langendorff and the work-performing isolated perfusion heart models, and (2) 31P NMR spectra to measure high energy metabolites. (Service 6) REPORT PERIOD: (09/01/97-08/31/98)

该项目的广泛长期目标是阐明 特定应力蛋白减少氧化损伤的机制， 并制定压力热冲击家族的策略 蛋白质可以增加缺血性心脏保护。 特定之一 目的是确定特定压力功能是否获得 在诱导系统的控制下，蛋白质表达将 通过效应挽救HSF1缺陷小鼠的缺血性敏感性 改善氧化应激/损害，增强心脏代谢， 并恢复心室功能。 我们已经开始研究以评估 使用（1）Langendorff和 绩效孤立的灌注心脏模型和（2）31p nmr 测量高能代谢产物的光谱。 （服务6）报告 周期：（09/01/97-08/31/98）