| Project/Area Number |
16K09578
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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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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Aichi Medical University (2017-2018)
Nagoya University (2016) |
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Principal Investigator |
Ito Satoru 愛知医科大学, 医学部, 准教授 (60378073)
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| Research Collaborator |
浅野 周一 名古屋大学, 大学院医学系研究科, 大学院生
高橋 光太 名古屋大学, 大学院医学系研究科, 大学院生
宮沢 亜矢子 名古屋大学, 大学院医学系研究科, 大学院生
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | メカニカルストレス / リモデリング / 気管支喘息 / 肺線維症 / 肺線維芽細胞 / 肺癌 / 気道平滑筋 / メカノバイオロジー / ストレッチ / 組織工学 / 肺線維化 / 喘息 / メカノトランスダクション / 細胞外基質 / 特発性肺線維症 / 基質硬度 |
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| Outline of Final Research Achievements |
We investigated mechanisms underlying substrate stiffness regulates cellular functions.
In human lung fibroblasts, migration and differentiation to myofibroblasts were enhanced by stiff substrate.
Expression of PD-L1 and cell growth were affected by matrix stiffness in human lung cancer cells. It is suggested that stiffness as a tumor environment regulates PD-L1 expression, which leads to evasion of the immune system and tumor growth. Activation of lung fibroblasts by the stiff lung and positive feedback may be involved in the mechanisms of progression of pulmonary fibrosis.
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| Academic Significance and Societal Importance of the Research Achievements |
細胞が足場として利用している基質の硬度を感知する基質力覚検知機構を明らかにし、肺や気道の線維化やリモデリングや病態や肺がんの免疫逃避機構の機序を解明することを目的として研究を行った。
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