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Regulation by Oxidative Stress of CO-and NO-Mediated Signal Transduction in Vascular Cells

血管细胞中 CO 和 NO 介导的信号转导的氧化应激调节

基本信息

批准号：
09044253
负责人：
BANNAI Shiro
金额：
$ 1.73万
依托单位：
University of Tsukuba
依托单位国家：
日本
项目类别：
Grant-in-Aid for international Scientific Research
财政年份：
1997
资助国家：
日本
起止时间：
1997 至无数据
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09044253/
关键词：
oxidative stress carbon monoxide nitrogen monoxide vascular cells macrophages low-density lipoprotein

项目摘要

Carbon monoxide (CO) and nitric monoxide (NO) play an important role in the physiological regulation of vascular tone and pathogenesis of atherosclerosis. In the present study we have obtained the following results.1. In human vascular smooth muscle cells, the activity of heme oxygenase, which generates CO,was induced by oxidized LDL and oxidative stress in a time-and dose-dependent manner.2. In human endothelial cells, the transport activity of arginine was stimulated and the production of NO increased by culturing the cells in higher concentration of glucose.3. In mouse macrophages, heme oxygenase was induced by oxidized LDL.However, the transport activity of arginine remained unchanged and production of NO was undetectable by oxidized LDL.From these results, it is suggested that under oxidative stress conditions heme oxygenase induced by oxidative stress increases the production of CO whereas NO is not generated. It is likely that the regulation of CO production is different from that of NO production. CO may function as the modulator of vascular tone under the oxidative stress conditions which are different from those where NO functions. Manuscripts containing these results are in preparation for papers.In 1998 UK98 Festival supported by the governments of UK and Japan will be held in Japan. In the course of the present joint research, we agreed as one of the events of UK98 Festival to hold a symposium entitled "Regulation of antioxidant system in oxidative stress" at University of Tsukuba, November l998. The British Council has offered a financial support for this symposium.

一氧化碳(CO)和一氧化氮(NO)在血管张力的生理调节和动脉粥样硬化的发病机制中起着重要作用。在本研究中，我们得到了以下结果：1.在人血管平滑肌细胞中，氧化型低密度脂蛋白和氧化应激以时间和剂量依赖的方式诱导产生一氧化碳的血红素加氧酶的活性。在人内皮细胞中，高浓度葡萄糖培养可刺激精氨酸的转运活性，增加NO的产生。氧化低密度脂蛋白可诱导小鼠巨噬细胞产生血红素加氧酶，但精氨酸的转运活性不变，氧化低密度脂蛋白不能检测到NO的产生。这些结果表明，在氧化应激条件下，氧化应激诱导的血红素加氧酶增加CO的产生，而NO不产生。CO产生的调节可能与NO产生的调节不同。在氧化应激条件下，CO可能作为血管张力的调节器发挥作用，而氧化应激条件不同于没有任何作用的情况。包含这些结果的手稿正在为论文做准备。1998年，由英国和日本政府支持的UK98艺术节将在日本举行。在目前的联合研究过程中，我们同意作为UK98节日的一项活动，于1998年11月在筑波大学举行题为“氧化应激中抗氧化系统的调节”的研讨会。英国文化协会为这次研讨会提供了财政支持。