| Project/Area Number |
24650250
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YAMAMOTO Kimiko 東京大学, 医学(系)研究科(研究院), 講師 (00323618)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 流れ剪断応力 / LDLコレステロール / 動脈硬化 / 血管内皮細胞 / 乱流 / 完全長cDNAライブラリー / 発現クローニング |
|---|
| Research Abstract |
LDL receptors, which were related to the onset of atherosclerosis caused vascular diseases such as the myocardial infarction or the cerebral infarction, were cloned. Although the pathological findings, which the atherosclerosis frequently appears on the endothelial cells exposed to turbulent fluid shear stress in the vascular bifurcation, were widely known, the details of the molecular mechanism were not fully apparent. Two kinds of clones that the mRNA and protein expression levels were down-regulated in response to laminar shear stress whereas those expression levels were up-regulated in response to turbulent shear stress were identified in human vascular endothelial cells by using a full-length cDNA library. The immunostaining study was confirmed that these two kinds of protein were expressed in human atherosclerotic lesions. These results indicate that the molecules discovered in this study play an important role in the mechanism of the onset of atherosclerosis.
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