Elucidation of the molecular mechanism of aorta dissection using perlecan deficient mice.
| Project/Area Number |
24790783
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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 |
Circulatory organs internal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
NONAKA RISA 順天堂大学, 医学(系)研究科(研究院), 研究員 (90614248)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 細胞外マトリックス / 基底膜分子パールカン / 大動脈内皮機能 / 中膜弾性線維層 / 血管内皮細胞 |
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| Outline of Final Research Achievements |
A deficiency of perlecan, a basement membrane component, in aorta tissue caused a decrease in endothelium-dependent relaxation function, and a reduced expression of endothelial NO synthase (eNOS) in aortic tissue. In addition, knockdown of perlecan in Human Aortic Endothelial Cells (HAEC) also showed reduced expression of eNOS. The reduced expression of eNOS was recovered in the presence of recombinant perlecan protein. These data suggest that the deficiency of perlecan in the aortic tissue leads to endothelial dysfunction, as represented by a reduction in endothelium-dependent relaxation. This dysfunction is due, at least partly, to a reduction in eNOS expression. In summary, our results showed that perlecan plays a role in maintaining the eNOS gene expression, and therefore in the endothelium-dependent relaxation function in the aorta.
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Report
(4 results)
Research Products
(8 results)
