| Project/Area Number |
08670817
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka City University |
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Principal Investigator |
KOHNO Masakazu Osaka City University, Medical School, Assistant Professor, 医学部, 講師 (20153489)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIKAWA Junichi Osaka City University, Medical School, Professor, 医学部, 教授 (60275245)
YASUNARI Kenichi Osaka City University, Medical School, Assistant, 医学部, 助手 (90231646)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | endothelin / vascular smooth muscle cell / proliferation / migration / coronary atherosclerosis / endothelin receptor |
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| Research Abstract |
Enidothelin (ET-1) is a vasoconstrictive and growth-promoting peptide that was firstly isolated from porcine vascular endothelial cells. Plasma ET-1 levels were shown to be increased in patients with symptomatic atherosclerotic vascular disease and hyperlipidemia. In the current study, we found that lysophosphatidylcholine, a prominent component of oxidized LDL, induces human coronary artery SMC migration and this lyso-PC-induced migration can be further induced by ET-1. Er_A receptor antagonist inhibited this enhancement by ET-1. We also found that lyso-PC stimulated ET-1 production in curltured human coronary artery SMC.ET-1 may recruit medial SMC during the process of coronary atherosclerosis in concert with oxidized LDL (lyso-PC) in vascular tissues. The conversion of phosphatidyicholine of LDL into lyso-PC during oxidized modification and ET-1 in atherosclerotic arterial wall may contribute to coronary atherogenesis. especiafly to the initial step of this disorder. Therefore, interventions that prevent this conversation in vivo and ET antagonism may be predicted to act to reduce coronary artery medial SMC_s into the intima in various pathophysiological settings.
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