Mechanisms of Macrophage Foam Cell Formation and Hypertensive Complications Caused by Vasoactive Agents
| Project/Area Number |
18590824
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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 | Showa University |
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Principal Investigator |
WATANABE Takuya Showa University, Biochemistry, Associate Professor (30297014)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAZAKI Akira Showa University, Biochemistry, Professor (70253721)
HIRANO Tsutomu Showa University, Internal Medicine, Professor (00167610)
鹿目 知子 昭和大学, 医学部, 研究員 (70420908)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,850,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥450,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2006: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Vasoactive Agents / Hypertension / Atherosclerosis / Complications / Urotensin ll / Salusin / Macrophage Foam Cell Formation / マクロファージ / 高血圧合併症 |
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| Research Abstract |
The present study clarified the mechanisms of macrophage foam cell formation and atherosclerosis caused by new vasoactive agents, such as urotensin II and salusins. Further, we studied the relationships between these vasoactive agents and hypertension or atherosclerotic diseases.
Urotensin II, the most potent vasoconstrictor peptide to date, accelerated foam cell formation via up-regulating acyl-CoA: cholesterol acyltransferase-1 (ACAT1) inhumanmonocyte-derivedmacrophages. Urotensin II also stimulated vascular smooth muscle cell (VSMC) proliferation with synergistic effects observed when combined with serotonin, oxidized low-density lipoprotein, or reactive oxygen species. In patients with essential hypertension, plasma levels of urotensin II were positively correlated with systolic blood 〓.the same precursor (prepro-salusin), were recently discovered as new vasoactive peptides. Salusin-β exerted the potent hypotensive effects. Human macrophage foam cell formation was enhanced by salusin-β via up-regulating ACAT1, whereas was reduced by salusin-a via down-regulating ACAT1. Immunoreactive salusin-a and salusin-β were detected in human coronary atherosclerotic plaques, with dominance of salusin-β in VSMCs, fibroblasts, and macrophage-foam cells. Serum levels of salusin-a were decreased in patients with acute coronary syndrome (ACS), stable effort angina pectoris, or post myocardial infarction than in hypertensive patients or healthy volunteers. Among these groups, serum salusin-α levels were the lowest in ACS patients and their salusin-α levels were decreased in accordance with the severity of coronary artery lesions. Serum salusin-α levels in hypertensive patients were slightly lower compared with that in healthy volunteers, and were negatively correlated with the severity of carotid 〓 findings suggest that vasoactive agents modulate the progression of atherosclerosis in hypertension and may be a candidate for biomarkers of atherosclerotic diseases.
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Report
(3 results)
Research Products
(27 results)
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[Presentation] Increased human urotensin II levels are correlated with carotid atherosclerosis in 〓2006
Author(s)
Suguro, T., Watanabe, T., Hirano, T., Miyazaki, A., et. al.
Organizer
American Heart Association Scientific Sessions 2006
Place of Presentation
Chicago, Illinois, USA
Description
「研究成果報告書概要(欧文)」より
Related Report
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