The role of mechanosensor molecule TRPV2 during monocyte transmigration across vascular endothelium in atherogenesis.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25350544
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biomedical engineering/Biomaterial science and engineering
• Research Institution: Kawasaki Medical School
• Principal Investigator: Hashimoto Ken 川崎医科大学, 医学部, 講師 (80341080)
• Co-Investigator(Kenkyū-buntansha): Mohri Satoshi 川崎医科大学, 医学部, 教授 (00294413) ; Ujihara Yoshihiro 川崎医科大学, 医学部, 助教 (80610021)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 動脈硬化 / 血管内皮細胞 / 単球 / 浸潤 / TRPV2 / メカノセンサー

Outline of Final Research Achievements

Adhesion and subsequent transmigration of blood monocytes across vascular endothelial cells are critical in early atherogenesis. We focused on the physical and mechanical interaction of monocytes and endothelial cells, and examined the role of TRPV2, Ca2+-permeable mechanosensor molecule expressed in endothelial cells. Biochemical analysis including TRPV2 knockdown and overexpression system revealed that TRPV2 is an essential molecule for cell survival by promoting cell migration and proliferation. It promotes cell migration by facilitating pseudopodium formation at the cell membrane through regulating actin cytoskeleton. The role of TRPV2 in the context of monocyte-endothelial interaction during transmigration is the subject of future study.

Free Research Field

動脈硬化、血管内皮、心臓生理学