Research for CD36 expression on vascular endothelial cells in atherogenesis
| Project/Area Number |
17590339
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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 |
Experimental pathology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
IWASA Satoshi University of Yamanashi, University of yamanashi Hospital, Assistant Professor (40328745)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥2,340,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥240,000)
Fiscal Year 2007: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2006: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | atherosclerosis / vascular endothelial cells / modified apolipoprotein / scavenger receptor / 循環器・高血圧 / 生理活性 / 細胞・組織 / 病理学 |
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| Research Abstract |
To elucidate the pathophysiological roles of CD36 in atherogenesis, I examined the expression pattern of CD36 and HO-1 proteins using human arteries and aortas of the murine model of atherosclerosis..
A few vascular endothelial cells expressed CD36 on the shoulder of the atheoma or orifices of aorta. CD36 expression on the endothelial cells was not induced by cholesterol-rich diet. Therefore, blood flow (shear-stress) may modulate endothelial CD36 expression.
In the stable atheroma, CD36 expression was almost restricted in the necrotic core, and viable foam cells abundantly expressed HO-1. However, in the ruptured plaque, foam cells tended to express stronger CD36, and weaker HO-1. This finding indicates that CD36 expression of foam cells may be involved in vulnerability of the plaques.
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Report
(4 results)
Research Products
(11 results)
