| Project/Area Number |
18K06200
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 44010:Cell biology-related
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| 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 / フィブロネクチン / LMO7 / 正常線維芽細胞 / 細胞の不死化 / 細胞形態 / 細胞間コミュニケーション |
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| 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.
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| 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。
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