Cooperative action of APJ and alpha1A-adrenrgic receptor in vascular smooth muscle cells induces intensive vasoconstriction

2016 Fiscal Year Final Research Report

• Project/Area Number: 26430086
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Laboratory animal science
• Research Institution: University of Tsukuba
• Principal Investigator: ISHIDA Junji 筑波大学, 生命領域学際研究センター, 講師 (30323257)
• Co-Investigator(Renkei-kenkyūsha): YAGAMI Ken-ichi 筑波大学, 医学医療系, 教授 (40166476) ; SUGIYAMA Fumihiro 筑波大学, 医学医療系, 教授 (90226481)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: APJ受容体 / 血管収縮 / アドレナリン受容体 / トランスジェニックマウス / ノックアウトマウス / シグナル伝達 / 受容体間相互作用

Outline of Final Research Achievements

APJ is a G protein-coupled receptor and highly expressed in various cardiovascular tissues. Although the physiological function of APJ on vascular endothelial cells was identified as a hypotensive system, its action on vascular smooth muscle cells (VSMCs) is still unclear. To examine the physiological role of APJ on VSMCs, we generated transgenic mice expressing APJ specifically in VSMCs, called SMA-APJ. Interestingly, I found sustained bradycardia and the development of coronary stenosis in SMA-APJ following apelin administration. An ex vivo assay using the Easy Magnus System revealed that the aorta of SMA-APJ was contracted intensively when co-stimulated with apelin and noradrenaline, a ligand of α1-adrenergic receptor (α1-AR).

Free Research Field

生化学　発生工学