Basic research for development of therapeutic strategy against atherosclerosis targeting interendothelial adhesion
Project/Area Number |
22590828
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | Kobe University |
Principal Investigator |
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 分子血管病態学 / 動脈硬化 / 接着分子 / 血管新生 / 血管平滑筋細胞 / 血管石灰化 / シグナル伝達 / Necl-5 / 血管内皮細胞 / 血管内皮増殖因子 / Rap1 / アファディン |
Research Abstract |
Necl-5, an immunoglobulin-like molecule, and afadin, an actin-binding protein, regulated tube formation, migration, proliferation and survival of vascular endothelial cells by controlling VEGF-induced activation of the Rap1-Akt signaling. Angiogenesis following femoral artery excision was reduced in Necl-5-knockout and endothelium-specific afadin-knockout mice. Our study revealed that Necl-5 and afadin in endothelial cells regulate angiogenesis.
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Report
(4 results)
Research Products
(26 results)