| Project/Area Number |
20591084
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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 |
Metabolomics
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| Research Institution | Showa University |
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Principal Investigator |
MIYAZAKI Akira Showa University, 医学部, 教授 (70253721)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Takuya 東京薬科大学, 生命科学部, 教授 (30297014)
HIRANO Tsutomu 昭和大学, 医学部, 教授 (00167610)
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| Co-Investigator(Renkei-kenkyūsha) |
SHICHIRI Masayoshi 北里大学, 医学部, 教授 (10206097)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
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| Keywords | 動脈硬化 / 血管作動性物質 / マクロファージ / 高血圧 / 単球 / 内皮細胞 / サリューシン / 接着分子 / 蛋白質 / コレステロール / 酵素 |
|---|
| Research Abstract |
Continuous subcutaneous infusion of urotensin II, a strong vasoconstrictor peptide, enhanced atherosclerotic lesions by 8-fold in fat-fed apoE-knockout mice. Analyses of peritoneal macrophages from urotensin II-treated mice revealed 7-fold increase in foam cell formation induced by oxidized LDL. Salusins are novel vasoregulatory peptides that derive from the same precursor. Development of atherosclerosis in apoE-KO mice was suppressed by 68% by continuous subcutaneous infusion of salusin-α but was 2.6-fold enhanced by salusin-β. Peritoneal macrophages from salusin?α-treated mice revealed 68% reduction in foam cell formation induced by oxidized LDL whereas macrophages from salusin-β-treated mice showed 2.6-fold increase in foam cell formation. Thus, urotensin II and salusins can be regarded as novel therapeutic targets for atherosclerosis.
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