The role of JCAD, an adhesion molecule of endothelial cell, in regulating cardiovascular disease

2015 Fiscal Year Final Research Report

• 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)
• 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
• Keywords: JCAD

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.

Free Research Field

循環器内科