Clarification of the mechanisms of cardiovascular dysfunction and the resultant organ failure
阐明心血管功能障碍和由此导致的器官衰竭的机制
基本信息
- 批准号:18390078
- 负责人:
- 金额:$ 10.77万
- 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:2006
- 资助国家:日本
- 起止时间:2006 至 2007
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Accumulating evidence suggests significance of the oxidized LDL receptor LOX-1 in endothelial and vascular dysfunction. In this study, we generated LOX-1 KO mice to address the role of LOX-1 in atherosclerotic diseases. With the KO mice, we obtained following results. (1) LOX-1 KO mice were resistant to the suppressive effects of oxidized LDL on endothelium-dependent relaxation. (2) Atherosclerosis induced by high fat diet was delayed in LOX-1 KO mice compared with wild type mice in both C57BL/6 and LDLRKO-C57BL/6 background. (3) Myocardial infarction and cardiac remodeling induced by LASD ligation was suppressed and cardiac function was relatively preserved in LOX-1 KO mice compared with wild type. (4) Both platelet aggregation in vitro and FeC12-induced thrombosis in vivo were suppressed in LOX-1 KO mice compared with wild type. Thus, we have demonstrated that LOX-1 aggravates every phase of atherosclerotic diseases, i.e. endothelial dysfunction, atherosclerosis, thrombosis, and myocardial infarction.
越来越多的证据表明氧化 LDL 受体 LOX-1 在内皮和血管功能障碍中的重要性。在这项研究中,我们培育了 LOX-1 KO 小鼠,以研究 LOX-1 在动脉粥样硬化疾病中的作用。通过 KO 小鼠,我们获得了以下结果。 (1) LOX-1 KO 小鼠对氧化 LDL 对内皮依赖性舒张的抑制作用具有抵抗力。 (2)在C57BL/6和LDLRKO-C57BL/6背景下,与野生型小鼠相比,LOX-1 KO小鼠高脂饮食诱导的动脉粥样硬化延迟。 (3)与野生型相比,LOX-1 KO小鼠LASD结扎诱导的心肌梗死和心脏重塑受到抑制,心功能相对保留。 (4)与野生型相比,LOX-1 KO小鼠体外血小板聚集和FeCl2诱导的体内血栓形成均受到抑制。因此,我们证明LOX-1会加重动脉粥样硬化疾病的各个阶段,即内皮功能障碍、动脉粥样硬化、血栓形成和心肌梗塞。
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)
Cyclic tensile stretch load and oxidized low density lipoprotein synergistically induce lectin-like oxidized LDL receptor-1 in cultured bovine chondrocytes, resulting in decreased cell viability and proteoglycan synthesis
- DOI:10.1002/jor.20211
- 发表时间:2006-08-01
- 期刊:
- 影响因子:2.8
- 作者:Akagi, Masao;Nishimura, Shunji;Hamanishi, Chiaki
- 通讯作者:Hamanishi, Chiaki
Oxidized LDL binding to LOX-1upregulates VEGF expression in cultured bovine chondrocytes through activation of PPAR-gamma.
氧化 LDL 与 LOX-1 结合,通过激活 PPAR-gamma 上调培养牛软骨细胞中 VEGF 的表达。
- DOI:
- 发表时间:2006
- 期刊:
- 影响因子:0
- 作者:Kanata;S
- 通讯作者:S
LOX-1 deletion alters signals of myocardial remodeling immediately after ischemia-reperfusion
- DOI:10.1016/j.cardiores.2007.07.003
- 发表时间:2007-11-01
- 期刊:
- 影响因子:10.8
- 作者:Hu, Changping;Dandapat, Abhijit;Mehta, Jawahar L.
- 通讯作者:Mehta, Jawahar L.
Lectin-like oxidized LDL receptor-1 as extracellular chaperone receptor : Its versatile functions and human diseases.
凝集素样氧化 LDL 受体 1 作为细胞外伴侣受体:其多功能功能与人类疾病。
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:Inoue;N. and Sawamura;T.
- 通讯作者:T.
Dominant-Negative Lox-1 Blocks Homodimerization of Wild-Type Lox-1–Induced Cell Proliferation Through Extracellular Signal Regulated Kinase 1/2 Activation
- DOI:10.1161/01.hyp.0000229825.98545.5e
- 发表时间:2006-08
- 期刊:
- 影响因子:8.3
- 作者:H. Tanigawa;S. Miura;Yoshino Matsuo;M. Fujino;T. Sawamura;K. Saku
- 通讯作者:H. Tanigawa;S. Miura;Yoshino Matsuo;M. Fujino;T. Sawamura;K. Saku
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SAWAMURA Tatsuya其他文献
SAWAMURA Tatsuya的其他文献
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{{ truncateString('SAWAMURA Tatsuya', 18)}}的其他基金
Elucidation of physiological significance of LOX-1 binding molecules
LOX-1结合分子的生理意义的阐明
- 批准号:
25293063 - 财政年份:2013
- 资助金额:
$ 10.77万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Pathophysiological significance of the factor which enhances the action of oxidized LDL, platelets, and leukocytes on vascular wall.
增强氧化低密度脂蛋白、血小板和白细胞对血管壁作用的因子的病理生理学意义。
- 批准号:
22390051 - 财政年份:2010
- 资助金额:
$ 10.77万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
STUDY ON THE SIGNIFICANCE OF LOX-1 IN OXIDATIVE STRESS-RELATED BIOLOGICAL RESPONSES
LOX-1在氧化应激相关生物反应中的意义研究
- 批准号:
16390070 - 财政年份:2004
- 资助金额:
$ 10.77万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Investigations for developing novel diagnostic methods, therapeutics, and drugs utilizing lectin-like oxidized LDL receptor-1 (LOX-1)
利用凝集素样氧化 LDL 受体 1 (LOX-1) 开发新型诊断方法、治疗方法和药物的研究
- 批准号:
11557006 - 财政年份:1999
- 资助金额:
$ 10.77万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
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