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Molecular Pathologic Study on Roles of Oxidative Stress in Thrombogenesis in Acute Coronary Syndrome

氧化应激在急性冠脉综合征血栓形成中作用的分子病理学研究

基本信息

批准号：
18590339
负责人：
UEDA Makiko
金额：
$ 2.55万
依托单位：
Osaka City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18590339/
关键词：
Acute Coronary Syndrome Coronary Thrombus Oxidative stress Neutrophil Myeloperoxidase Neopterin S100A8 A9 血小板

项目摘要

The aim of the present study was to clarify the significance and roles of oxidative stress in the pathogenesis of thrombus formation and progression leading to the development of acute coronary syndromes. In particular, in the present study, we investigated the relationships between myeloperoxidase, oxidized LDL, and other oxidation-related substances.In the first year, we clarified that intraplaque hemorrhage induces oxidative stress in human unstable coronary plaques obtained by atherectomy(Circulation, 114: 744S, 2006),and also revealed new findings on the immunolocalization of platelet glycoprotein IIb/IIIa, P-selectin, and neutrophil-platelet association in human carotid unstable plaques(J Am Coll Cardiol 49: 406A, 2007).We also reported the relationship between thrombosis at the site of unstable plaques and oxidative stress in patients with acute coronary syndromes(Atherosler Thromb Vas Biol, 26: 877-883, 2006).In the second year, we extended the research objects to clarify the relationship between neutrophil myeloperoxidase and oxidation-related biomarkers including neopterin and S100 A8/A9 complex. We demonstrated the significance of neopterin and oxidative stress in plaque inflammation and destabilization of human coronary atherosclerotic lesions(Heart 93: 1537-1541, 2007).We moreover revealed the participation of S100 A8/A9 complex, which was involved in the inflammatory process of coronary atherosclerosis in patients with acute coronary syndromes(Heart, 2008, in press).

本研究的目的是阐明氧化应激在血栓形成和进展导致急性冠状动脉综合征的发病机制中的意义和作用。在本研究中，我们特别研究了髓过氧化物酶、氧化低密度脂蛋白和其他氧化相关物质之间的关系。在第一年，我们阐明了斑块内出血可诱导斑块切除术获得的不稳定冠状动脉斑块中的氧化应激（《循环》，114：744 S，2006），并且还揭示了关于血小板糖蛋白IIb/IIIa，P-选择素，人颈动脉不稳定斑块中的血小板-嗜中性粒细胞相关性（J Am科尔Cardiol 49：406 A，2007）。我们还报道了急性冠脉综合征患者不稳定斑块部位血栓形成与氧化应激之间的关系（Atherosler Thromb Vas Biol，26：877-883，2006）。第二年，我们将研究对象扩展到阐明中性粒细胞髓过氧化物酶与氧化相关生物标志物包括新蝶呤和S100 A8/A9复合物之间的关系。我们证明了新蝶呤和氧化应激在人冠状动脉粥样硬化病变的斑块炎症和不稳定中的重要性（Heart 93：1537-1541，2007），我们还揭示了S100 A8/A9复合物的参与，其参与急性冠状动脉综合征患者冠状动脉粥样硬化的炎症过程（Heart，2008，出版中）。