Base construction for the development of therapeutic strategies for targeting cell adhesion molecules in atherosclerosis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461128
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Kobe Pharmaceutical University (2015); Kobe University (2013-2014)
• Principal Investigator: Rikitake Yoshiyuki 神戸薬科大学, 薬学部, 教授 (50419488)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 細胞接着分子 / 血管内皮細胞 / シグナル伝達 / 内膜肥厚 / 血管炎症

Outline of Final Research Achievements

The following findings were obtained by analyzing the functions and mode of action of cell adhesion molecules in atherosclerosis. (1) Necl-5 facilitated dedifferentiation of smooth muscle cells from a contractile to a synthetic phenotype, cell movement and proliferation, and intimal thickening after the common carotid artery ligation. (2) Necl-4, whose expression increased as vascular endothelial cells become confluent, induced contact inhibition of movement and proliferation by suppressing autophosphorylation of the vascular endothelial growth factor receptor via PTPN13. (3) In vascular endothelial cells FAM5C increased in response to inflammatory stimuli and promoted expression of monocyte adhesion molecules via enhanced production of reactive oxygen species and activation of NF-kappa B.

Free Research Field

血管細胞生物学