MECHANISM OF MITOCHONDRIAL K_<ATP> CHANNEL-MEDIATED CARDIOPROTECTION
线粒体 K_<ATP> 通道介导的心脏保护机制
基本信息
- 批准号:13670044
- 负责人:
- 金额:$ 2.3万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2001
- 资助国家:日本
- 起止时间:2001 至 2002
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
MITOCHONDRIAL ATP-SENSITIVE POTASSIUM (MITO-K_<ATP>) CHANNELS ARE THOUGHT TO PLAY A KEY ROLE IN ISCHEMIC PRECONDITIONING. THIS STUDY WAS UNDERTAKEN TO KNOW THE MECHANISM OF MITO-K_<ATP> CHANNEL-MEDIATED CARDIOPROTECTION. THE RESULTS OF THIS INVESTIGATION ARE AS FOLLOWS.(1) OPENING OF MITO-K_<ATP> CHANNELS BY DIAZOXIDE DEPOLARIZED THE MITOCHONDRIAL MEMBRANE POTENTIAL AND THEREBY PRIVENTING THE MITOCHONDRIAL CALCIUM OVERLOAD. OTHER MITO-K_<ATP> CHANNEL OPENERS, NICORANDIL AND MINOXIDIL, SIMILARLY ATTENUATED THE MITOCHONDRIAL CALCIUM OVERLOAD.(2) THE KIR6.2-DEFICIENT MOUSE HEARTS IN VIVO LACK THE INFARCT SIZE-LIMITING EFFECT OF ISCHEMIC PRECONDITIONING. HOWEVER, ACTIVATION OF MITO-K_<ATP> CHANNELS BY DIAZOXIDE PROTECTED THE QUIESCENT CARDIOMYOCYTES FROM MITOCHONDRIAL CALCIUM OVERLOAD IN BOTH KIR6.2- AND KIR6.1-DEFICIENT MICE.(3) PRETREATMENT OF CARDIOMYOCYTES WITH DIAZOXIDE FOR 30 MINUTES PRIOR TO EXPOSURE TO H_2O_2 ELICITED THE TRANSIENT DEPOLARIZATION OF MITOCHONDRIAL MEMBRANE POTENTIAL, AND CONSEQUENTLY SUPPRESSED APOPTOSIS AFTER 2 HOURS EXPOSURE TO H_2O_2.THESE RESULTS, TAKEN TOGETHER, SUGGEST THAT OPENING OF MITO-KATP CHANNELS 1) PREVENTS A MITOCHONDRIAL CALCIUM OVERLOAD IN ASSOCIATION WITH DEPOLARIZATION OF MITOCHONDRIAL MEMBRANE POTENTIAL, 2) TRIGGERS CARDIOPROTECTION AGAINST APOPTOSIS INDUCED BY OXIDATIVE STRESS.
线粒体ATP敏感性钾<ATP>通道在缺血预适应中起重要作用。本研究旨在探讨线粒体钾<ATP>通道介导的心肌保护作用的机制。调查结果如下。(1)二氮嗪开放线粒体K_2<ATP>通道使线粒体膜电位去极化,从而抑制线粒体钙超载。其他MITO-K_<ATP>通道开放剂尼可地尔和米诺地尔也可类似地减轻线粒体钙超载。(2)KIR6.2缺陷小鼠体内心脏缺乏缺血预处理的梗死面积限制效应。但是,二氮嗪激活线粒体K_2<ATP>通道可使KIR6.2和KIR6.1缺陷小鼠静息心肌细胞免于线粒体钙超载。(3)在暴露于H_2O_2前用二氮嗪预处理心肌细胞30分钟,可引起线粒体膜电位的一过性去极化,而暴露于H_2O_2后2小时,细胞凋亡受到抑制。这些结果表明:1)线粒体KATP通道的开放可防止与线粒体膜电位去极化有关的线粒体钙超载,2)触发抗氧化应激诱导的细胞凋亡的心脏保护作用。
项目成果
期刊论文数量(23)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
SUZUKI M, SAITO T, SATO T. TAMAGAWA M, MIKI T, SEINO S, NAKAYA H.: "CARDIOPROTECTIVE EFFECT OF DIAZOXIDE IS MEDIATED BY ACTIVATION OF SARCOLEMMAL BUT NOT MITOCHONDRIAL ATP-SENSITIVE K^+ CHANNELS IN MICE"CIRCULATION. 107. 682-685 (2003)
SUZUKI M、SAITO T、SATO T. TAMAGAWA M、MIKI T、SEINO S、NAKAYA H.:“二氮氧化物的心脏保护作用是通过激活小鼠肌膜而不是线粒体 ATP 敏感 K^ 通道来介导的”循环。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
SUZUKI M, SASAKI N, MIKI T, SAKAMOTO N. OHMOTO-SEKINE Y, TAMAGAHA M, SEINO S, MARBAN E, NAKAYA H.: "ROLE OF SARCOLEMMAL K_<ATP> CHANNELS IN CARDIOPROTECTION AGAINST ISCHEMIA/REPERFUSION INJURY IN MICE"J CLIN INVEST. 109. 509-516 (2002)
SUZUKI M, SASAKI N, MIKI T, SAKAMOTO N. OHMOTO-SEKINE Y, TAMAGAHA M, SEINO S, MARBAN E, NAKAYA H.:“肌膜 K_<ATP> 通道在针对小鼠缺血/再灌注损伤的心脏保护中的作用”J
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Ishida H: "Opening of mitochondrial K_<ATP> channels attenuates the ouabain-induced calcium overload in mitochondria"Circulation Research. 89. 856-858 (2001)
Ishida H:“线粒体 K_<ATP> 通道的开放可减弱哇巴因诱导的线粒体钙超载”循环研究。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Ishida H, et al.: "Opening of mitochondrial K_<ATP> channels attenuates the ouabain-induced calcium overload in mitochondria"Circulation Research. 89. 856-858 (2001)
Ishida H 等人:“线粒体 K_<ATP> 通道的开放可减弱哇巴因诱导的线粒体钙超载”循环研究。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Suzuki M: "Functional roles of cardiac and vascular ATP-sensitive potassium channels clarified by Kir6.2-knockout mice"Circulation Research. 88. 570-577 (2001)
Suzuki M:“Kir6.2 敲除小鼠阐明了心脏和血管 ATP 敏感钾通道的功能作用”循环研究。
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- 影响因子:0
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