Prevention of atherosclerotic plaque rupture by the regulation of oxygen radical metabolism of vascular wall cells.
通过调节血管壁细胞氧自由基代谢预防动脉粥样硬化斑块破裂。
基本信息
- 批准号:10557071
- 负责人:
- 金额:$ 8.64万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 财政年份:1998
- 资助国家:日本
- 起止时间:1998 至 1999
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Recent studies revealed that myocardial infarction is not occurred from highly progressive atherosclerotic lesions, but rather from relatively mild lesions. Therefore, prevention of rupture of unstable coronary plaque is necessary for the prevention of acute myocardial infarction. In this study, we examined whether regulation of oxygen radical in vascular smooth muscle cells can modulate stability of atherosclerotic plaque. In the first year, we demonstrated that antioxidative enzyme, Mn-SOS, was induced in cultured vascular smooth muscle cells by the preconditioning with heat shock or TNF-α together with the acquisition of tolerance to oxidative stress. In the second year, we revealed that the induction of Mn-SOD by TNF-α was inhibited by the addition of antisenseoligodeoxyribonucleotide (AODN) to Mn-SOD and that the tolerance to oxidative stress was also abolished by the treatment with AODN. On the other hand, lipofection of Mn-SOD to smooth muscle cells introduced Mn-SOD in mitochondria of cells and augmented tolerance to oxidative stress. These results suggest that the expression of antioxidative enzyme in vascular wall cells is closely related to the survival of smooth muscle cells and that by introducing antioxidative enzyme in cells could stabilize atherosclerotic plaque.
近年来的研究表明,心肌梗死并非发生于高度进展的动脉粥样硬化病变,而是发生于相对较轻的病变。因此,预防不稳定冠状动脉斑块破裂对预防急性心肌梗死是必要的。在这项研究中,我们研究了血管平滑肌细胞中氧自由基的调节是否可以调节动脉粥样硬化斑块的稳定性。在第一年,我们证明了在培养的血管平滑肌细胞中,通过热休克或TNF-α预处理诱导抗氧化酶Mn-SOS,并获得对氧化应激的耐受。第二年,我们发现在Mn-SOD中加入反义寡脱氧核苷酸(AODN)可以抑制TNF-α对Mn-SOD的诱导作用,并且AODN也可以消除Mn-SOD对氧化应激的耐受性。另一方面,脂质体转染Mn-SOD到平滑肌细胞中,将Mn-SOD引入细胞的线粒体中,并增强对氧化应激的耐受性。提示血管壁细胞抗氧化酶的表达与平滑肌细胞的存活密切相关,在细胞内导入抗氧化酶可稳定动脉粥样硬化斑块。
项目成果
期刊论文数量(26)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Ueda Y, Kitakaze M, Komamura K, et al.: "Pravastatin restored the infarct size-limiting effect of ischemic preconditioning blunted by hypercholesterolemia in the rabbit model of myocardial infarction"J. Am Coll Cardiol.. 34. 2120-2125 (1999)
Ueda Y、Kitakaze M、Komamura K 等人:“在兔心肌梗塞模型中,普伐他汀恢复了因高胆固醇血症而减弱的缺血预处理对梗塞面积的限制作用”,J.
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Ueda, Y., M. Kitakaze, M. lmakita. et al.: "Glycoprotein llb/llla antagonist FK633 could not1 prevent neointimal thickening in stent implantation model of canine coronary artery."Arterioscler. Thromb. Vasc. Biol.. 9. 343-347 (1999)
Ueda, Y.,M. Kitakaze,M. lmakita。
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Kitakaze, M., H. Funaya, K. Komamura et al.: "Nisoldipine selectively induces coronary vasodilation and improves mild myocardial ischemia in dogs : a potential role of cellular acidosis."Cardiovasc. Drugs Ther.. 12. 533-541 (1998)
Kitakaze, M., H. Funaya, K. Komamura 等人:“尼索地平选择性诱导冠状血管舒张并改善狗的轻度心肌缺血:细胞酸中毒的潜在作用。”心血管。
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- 影响因子:0
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Minamino, T., M. Kitakaze, H. Asanuma: "Endogenous adenosine inhibits P-selectin-dependent formation of coronary thromboemboli during hypoperfusion in dogs."J. Clin. Invest. 101. 1643-1653 (1998)
Minamino, T., M. Kitakaze, H. Asanuma:“内源性腺苷在狗灌注不足期间抑制 P-选择素依赖性冠状动脉血栓栓塞的形成。”J.
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Ueda Y. et al.: "Pravastatin restored the infarct size-limiting effect of ischemic preconditioning blunted by hypercholesterolemia in the rabbit model myocardial infarction"J Am Coll Cardiol. 34. 2120-2125 (1999)
Ueda Y.等人:“普伐他汀恢复了兔心肌梗塞模型中因高胆固醇血症而削弱的缺血预处理的梗塞面积限制作用”J Am Coll Cardiol。
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- 影响因子:0
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HORI Masatsugu其他文献
HORI Masatsugu的其他文献
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{{ truncateString('HORI Masatsugu', 18)}}的其他基金
Cardiac stress-responsive mechanism and its theraprutic application
心脏应激反应机制及其治疗应用
- 批准号:
11307013 - 财政年份:1999
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for Scientific Research (A).
Molecular epidemiology of acute coronary syndrome in Japan : Large-scale, prospective, multicenter clinical investigation
日本急性冠状动脉综合征的分子流行病学:大规模、前瞻性、多中心临床研究
- 批准号:
11794035 - 财政年份:1999
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for University and Society Collaboration
The pathophysiological significanse and mechanism of activation of key enzyme responsible for adenosine production in ischemic preconditioning.
缺血预处理中负责腺苷产生的关键酶的病理生理意义和激活机制。
- 批准号:
07457171 - 财政年份:1995
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Development of in vitro reconstituted system for investigating intracellular signal trasduction and cellular function in myocardial cells
开发用于研究心肌细胞内信号转导和细胞功能的体外重建系统
- 批准号:
07557057 - 财政年份:1995
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Role of calcium overload on coronary arterial stunning caused by myocardial ischemia reperfusion
钙超载对心肌缺血再灌注引起的冠状动脉顿抑的作用
- 批准号:
05670613 - 财政年份:1993
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Cardioprotective roles of adenosine against ischemic and reperfusion injury
腺苷对缺血和再灌注损伤的心脏保护作用
- 批准号:
03670449 - 财政年份:1991
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Role of Adrenergic Activity, Alpha-Receptor, and Beta-Receptor in Progression of Chronic Heart Failure
肾上腺素能活性、α 受体和 β 受体在慢性心力衰竭进展中的作用
- 批准号:
01570484 - 财政年份:1989
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Role of Neurohumoral Abnormalities and -Adrenergic Reeptor Changes in Progression of Chronic Heart Failure
神经体液异常和肾上腺素受体变化在慢性心力衰竭进展中的作用
- 批准号:
62570392 - 财政年份:1987
- 资助金额:
$ 8.64万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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