| Project/Area Number |
25860418
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Laboratory medicine
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
Sato Kengo 東京薬科大学, 生命科学部, 助教 (70549930)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 動脈硬化 / バイオマーカー / ペプチド / 血管内皮細胞 / マクロファージ / 血管平滑筋細胞 |
|---|
| Outline of Final Research Achievements |
Cardiotrophin-1 (CT-1) and kisspeptin-10 (KP-10) enhanced foam-cell formation, but urocortin (Ucn) and tumor necrosis factor-stimulated gene-6 (TSG-6) suppressed foam cell formation in human macrophages. The migration and proliferation were stimulated by CT-1, suppressed by Ucn and TSG-6 in human vascular smooth muscle cell. Ucn and TSG-6 suppressed LPS-induced up-regulation of MCP1, IL6, ICAM1, and VCAM1 in human umbilical vein endothelial cells (HUVECs). Four-week-infusion of CT-1 and KP-10 into apolipoprotein E-deficient mice accelerated the development of aortic atherosclerotic lesions, whereas Ucn and TSG-6 retarded the atherogenesis. In coronary artery disease (CAD) patients, plasma TSG-6 levels were increased and TSG-6 was highly expressed in the fibrous cap within coronary atherosclerotic plaques. Thus, TSG-6 can be regarded as a novel therapeutic target and TSG-6 may be a candidate for biomarkers of CAD.
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