OXYRADICALS, ADENOSINE, STRESS PROTEINS AND PRECONDITION
氧化自由基、腺苷、应激蛋白和预处理
基本信息
- 批准号:2445254
- 负责人:
- 金额:$ 16.77万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1995
- 资助国家:美国
- 起止时间:1995-08-01 至 1999-06-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION: (Adapted from abstract): Recent studies have shown that a
brief exposure to ischemia renders the heart better able to tolerate a
subsequent longer ischemic insult, a phenomenon called ischemic
preconditioning. The first hypothesis of this proposal is that ischemic
preconditioning is accompanied by enhanced and sustained gene expression
of HSPs in the heart of rats and rabbits. In addition to HSP70, the
applicants will explore the role of other stress proteins such as HSP27,
60, and 90. The second hypothesis is that quercitine, an inhibitor of
the heat shock transcription factor, blocks preconditioning by blocking
the synthesis of HSPs. The third hypothesis is that oxygen radicals
directly trigger the preconditioning and that scavenging of radicals by
antioxidants attenuates the protection derived from preconditioning and
reduces the expression of HSPs. The fourth hypothesis is that
activation of adenosine A1-receptors during preconditioning results in
enhanced expression of HSPs. The applicants will examine the effects of
adenosine agonists and antagonists on preconditioning and HSP synthesis
in rats as well as rabbits. The fifth hypothesis is that synthesis of
HSPs mediates the second window of protection which develops 24 hours
after ischemic preconditioning. The applicants anticipate answering the
following questions: (1) whether preconditioning induces the expression
of HSP27, 60, and 90 in addition to HSP70; (2) whether HSPs are involved
in preconditioning early or late; (3) whether oxygen radicals trigger
the preconditioning by inducing HSP; and (4) whether adenosine receptor
activation induces expression of HSPs resulting in preconditioning.
描述:(改编自摘要):最近的研究表明,
短暂暴露于局部缺血使心脏能够更好地耐受
随后更长时间的缺血性损伤,这种现象称为缺血性损伤,
预处理这个提议的第一个假设是,
预处理伴随着增强和持续的基因表达
大鼠和兔子心脏中的热休克蛋白。除了HSP 70,
申请人将探索其它应激蛋白如HSP 27的作用,
60和90。第二个假设是槲皮素,一种抑制剂,
热休克转录因子,通过阻断预处理,
热休克蛋白的合成。第三个假设是氧自由基
直接触发预处理和清除自由基,
抗氧化剂减弱来自预处理的保护,
减少HSPs的表达。第四个假设是,
在预处理过程中腺苷A1受体的激活导致
HSPs的表达增强。申请人将审查
腺苷激动剂和拮抗剂对预适应和HSP合成的影响
在老鼠和兔子身上。第五个假设是,
热休克蛋白介导的第二个保护窗口,发展24小时
缺血预处理后。申请人期望回答
以下问题:(1)预处理是否诱导表达
HSP 27、60、90与HSP 70的关系;(2)HSP 70与HSP 27、60、90的关系
预适应早期或晚期的氧自由基是否触发
诱导HSP预处理;(4)腺苷受体是否
活化诱导HSP的表达,导致预处理。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Rakesh C Kukreja其他文献
Sildenafil Citrate (Viagra) Induces Cardioprotective Effects after Ischemia/Reperfusion Injury in Infant Rabbits
柠檬酸西地那非(伟哥)可诱导幼兔缺血/再灌注损伤后的心脏保护作用
- DOI:
10.1203/01.pdr.0000147736.27672.15 - 发表时间:
2005-01-01 - 期刊:
- 影响因子:3.100
- 作者:
Yvonne A Bremer;Fadi Salloum;Ramzi Ockaili;Eric Chou;William B Moskowitz;Rakesh C Kukreja - 通讯作者:
Rakesh C Kukreja
Rakesh C Kukreja的其他文献
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{{ truncateString('Rakesh C Kukreja', 18)}}的其他基金
BMP-7 Modulates Inflammation induced cell death in Diabetic Cardiac and Skeletal Muscle
BMP-7 调节糖尿病心肌和骨骼肌炎症诱导的细胞死亡
- 批准号:
9788441 - 财政年份:2018
- 资助金额:
$ 16.77万 - 项目类别:
BMP-7 Modulates Inflammation induced cell death in Diabetic Cardiac and Skeletal Muscle
BMP-7 调节糖尿病心肌和骨骼肌炎症诱导的细胞死亡
- 批准号:
10242150 - 财政年份:2018
- 资助金额:
$ 16.77万 - 项目类别:
Amelioration of Doxorubicin Induced Muscle Dysfunction with Embryoinic stem cells-Derived Exosomes
利用胚胎干细胞来源的外泌体改善阿霉素引起的肌肉功能障碍
- 批准号:
10322656 - 财政年份:2018
- 资助金额:
$ 16.77万 - 项目类别:
BMP-7 Modulates Inflammation induced cell death in Diabetic Cardiac and Skeletal Muscle
BMP-7 调节糖尿病心肌和骨骼肌炎症诱导的细胞死亡
- 批准号:
10376557 - 财政年份:2018
- 资助金额:
$ 16.77万 - 项目类别:
ROS, Inflammation, and Cardioprotection in Type 2 Diabetes
2 型糖尿病中的 ROS、炎症和心脏保护
- 批准号:
8701394 - 财政年份:2013
- 资助金额:
$ 16.77万 - 项目类别:
ROS, Inflammation, and Cardioprotection in Type 2 Diabetes
2 型糖尿病中的 ROS、炎症和心脏保护
- 批准号:
8522552 - 财政年份:2013
- 资助金额:
$ 16.77万 - 项目类别:
Health Educational Research Opportunities (HERO)
健康教育研究机会(HERO)
- 批准号:
7797605 - 财政年份:2008
- 资助金额:
$ 16.77万 - 项目类别:
Health Educational Research Opportunities (HERO)
健康教育研究机会(HERO)
- 批准号:
7617652 - 财政年份:2008
- 资助金额:
$ 16.77万 - 项目类别:
Cardioprotective Signaling following Phosphodiesterase-5 Inhibition
磷酸二酯酶 5 抑制后的心脏保护信号传导
- 批准号:
8258744 - 财政年份:2008
- 资助金额:
$ 16.77万 - 项目类别:
Cardioprotective Signaling following Phosphodiesterase-5 Inhibition
磷酸二酯酶 5 抑制后的心脏保护信号传导
- 批准号:
7867829 - 财政年份:2008
- 资助金额:
$ 16.77万 - 项目类别:
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