The role of gap junction-mediated regulation of endothelial cellular stiffness

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K09513
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Shimane University
• Principal Investigator: Okamoto Takayuki 島根大学, 学術研究院医学・看護学系, 准教授 (30378286)
• Research Collaborator: Suzuki Koji ; Shimaoka Motomu ; Kawamoto Eiji ; Niibayashi Tomomi ; Usuda Haruki ; Tanaka Tetsuya ; Wada Koichiro
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 血管内皮細胞 / 細胞硬化 / ギャップ結合 / 細胞接着斑 / 細胞骨格 / 白血球接着

Outline of Final Research Achievements

The aim of this study is to investigate alteration in elastic modulus (stiffness) of vascular endothelial cells during inflammation using atomic force microscope, and to clarify the pathophysiological role of cellular stiffness. We found that vascular endothelial cells increased the stiffness during inflammatory stimulation. Here we have demonstrated that gap junction is involved in the regulation of cellular stiffness. Furthermore, we have shown that cellular stiffening induces leukocyte adhesion. Taken together, our results suggested the pathophysiological role of endothelial cellular stiffness.

Free Research Field

血管生物学、血栓止血学、細胞接着学、分子薬理学

Academic Significance and Societal Importance of the Research Achievements

臨床的には、血管が硬くなると動脈硬化が進展し、心血管イベントが生じやすいことが知られている。本研究では、そのメカニズムの解明に取り組み、病態初期に見られる炎症時において血管内皮細胞そのものが硬化することを示し、その分子機構を解析した。さらに細胞が硬化した結果、白血球が硬化部位に集積する可能性を示し、血管硬化が血管病変の形成を促進する新しいメカニズムを明らかにした。