Molecular mechanism that enables robust directional migration of normal fibroblasts

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K06200
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 44010:Cell biology-related
• Research Institution: Hokkaido University
• Principal Investigator: Takahashi Masayuki 北海道大学, 理学研究院, 特任教授 (50241295)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 細胞遊走 / 線維芽細胞 / 細胞骨格 / 接着斑 / 細胞間接着 / ミオシンII

Outline of Final Research Achievements

When cells reach a state of confluence in a culture dish, cell migration is stopped by a phenomenon called "contact inhibition of locomotion". Normal fibroblast cells can continue to migrate straight, smartly passing each other, even though they are in contact with other cells in the confluent state. To clarify the molecular mechanism of this persistent directional migration of normal fibroblast cells, we focused on the organization of the cytoskeleton and intercellular adhesion structure. We found that normal fibroblast cells did not form a rigid adhesive structure on the lateral sides where cells come into contact with each other in an aligned confluent state. We also found that myosin II proteins were highly activated on the lateral sides of the cell to prevent protrusion formation from there.

Free Research Field

生物化学

Academic Significance and Societal Importance of the Research Achievements

本研究によって、正常線維芽細胞が、コンフルエント状態においても強固に方向を持続した遊走を可能にする分子メカニズムの一端を明らかにすることができた。本研究成果が、細胞集団内での細胞間のコミュニケーションや細胞の運動様式を制御する新たな分子基盤の発見につながることが期待される。傷ができた際に、多数の線維芽細胞が傷口に集まりコラーゲンなどの細胞外マトリックス成分を分泌し傷を修復するが、本研究成果が、将来、新しい観点からの創傷治癒の薬剤の開発につながることも期待される。