Elucidation of the molecular mechanism underlying the vascular dysfunction mediated by proteinase-activated receptor 1

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09159
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Kyushu University
• Principal Investigator: Hirano Mayumi 九州大学, 医学研究院, 助教 (80336031)
• Co-Investigator(Kenkyū-buntansha): 平野 勝也 香川大学, 医学部, 教授 (80291516)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: プロテイナーゼ活性化型受容体(PAR1) / 血管内皮細胞 / 血管透過性 / 内皮バリアー障害 / ミオシン軽鎖リン酸化 / アクチン / 血管平滑筋細胞 / 肺高血圧症

Outline of Final Research Achievements

1. Myosin di-phosphorylation and peripheral actin bundle formation as initial events during endothelial barrier disruption. 2. The Rho-Rho kinase pathway plays an important role in the peripheral localization of ppMLC and actin filament formation during the initial phase of the thrombin-induced endothelial barrier disruption. 3. The coagulation factor XIa induces Ca2+ signal via proteinase-activated receptor 1(PAR1) and L-type Ca2+channel in vascular smooth muscle cells. 4. Specific and increased expression of thrombin receptor PAR1 in pulmonary artery plays a key role in the pathogenesis of monocrotaline-induced pulmonary hypertension in rats.

Free Research Field

医歯薬学　内科系臨床医学　循環器内科学　分子血管学