Project/Area Number |
25461129
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Cardiovascular medicine
|
Research Institution | Kobe University |
Principal Investigator |
kawai hiroya 神戸大学, 医学(系)研究科(研究院), 教授 (20346266)
|
Co-Investigator(Kenkyū-buntansha) |
ISHIDA TATSUEO 神戸大学, 医学研究科, 特命教授 (00379413)
杜 隆嗣 神戸大学, 医学(系)研究科(研究院), 准教授 (50379418)
|
Co-Investigator(Renkei-kenkyūsha) |
TOH RYUJI 神戸大学, 医学研究科, 特命准教授 (50379418)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | JCAD / angiogenesis / 血管内皮細胞 / 循環器 / 血管新生 / 動脈硬化 / 接着分子 / VE-カドヘリン |
Outline of Final Research Achievements |
Cell culture experiments revealed impaired angiogenic ability (proliferation, migration, and tube formation) by the knockdown of JCAD with siRNA. We have generated mice lacking JCAD (mKIAA1462 -/-) by gene-targeted deletion of JCAD to address in vivo angiogenic function. mKIAA1462-/- mice did not show morphological differences in development of retinal vasculature. Ex vivo aortic ring model demonstrated impaired neovascularization in aorta from mKIAA1462-/- mice than control wild-type mice (p<0.05). Tumor growth was assessed by monitoring tumor volume after the subcutaneous injection of melanoma cells into the mice. mKIAA1462-/- mice exhibited 45% smaller tumor volume compared with wild-type mice (p<0.001). Histological assessment of the tumor exhibited less smooth muscle actin (SMA)-positive neovascularization determined by CD31 staining in tumor of mKIAA1462-/- mice than wild-type mice, indicating that knockdown of JCAD inhibited the vascular maturation in angiogenic process.
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