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2018 Fiscal Year Final Research Report

Effects of cellular mechanical environment on response to interleukin-1beta stimulation in isolated tenocytes

Research Project

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Project/Area Number 16K01346
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Biomedical engineering/Biomaterial science and engineering
Research InstitutionNagoya University

Principal Investigator

Maeda Eijiro  名古屋大学, 工学研究科, 助教 (20581614)

Research Collaborator Kimura Shunsuke  
Project Period (FY) 2016-04-01 – 2019-03-31
Keywords腱 / 腱細胞 / 炎症応答制御 / 細胞張力 / 膜流動性 / インターロイキン1ベータ
Outline of Final Research Achievements

The present study investigated effects of cellular tension and cell membrane dynamics on responses to IL-1b stimulation in tenocytes isolated from rabbit Achilles tendon. The cells were subjected to IL-1b treatments on substrates with different stiffness, and their MMP-1 expression as well as the fluidity of cell membrane were examined. It has been demonstrated that the cells on substrate with lower stiffness exhibited higher expression of MMP-1 mRNA and lower membrane fluidity. Based on these findings, the following mechanism is suggested. When tenocytes are seeded on a substrate with low stiffness, cellular tension is lowered, which, in turn, decreases the fluidity of cell membrane proteins. This would elevate the special concentration of ligand receptors and these receptors form clusters, which could enhance the responsiveness of the receptors. This hypothetical mechanism indicates the importance of mechanical status of cells in regulating a wide range of cellular functions.

Free Research Field

バイオメカニクス,メカノバイオロジー

Academic Significance and Societal Importance of the Research Achievements

本研究の成果は,細胞周囲の力学環境が細胞の張力のみならず細胞膜の力学特性にも影響を及ぼし,それらは細胞外からの刺激因子に対する応答性に大きな影響を与えることを示した点にある.基板剛性に由来する細胞張力の低下は,過負荷による腱組織内での局所的な破断に伴って腱細胞から力学刺激が失われた状態に近いと考えられることから,本研究で示唆された機序は過負荷が作用した腱組織において組織分解・変性が発症・進行するメカニズムを示唆するものと考えられる.このことから,それらの症状に対して細胞張力や細胞力学環境に焦点を当てた予防法や治療法が有効であることを示した.

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Published: 2020-03-30  

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