| Project/Area Number |
26560207
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biomedical engineering/Biomaterial science and engineering
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| Research Institution | Ibaraki University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUMOTO TAKEO 名古屋工業大学, 大学院工学研究科, 教授 (30209639)
SUGITA SHUKEI 名古屋工業大学, 大学院工学研究科, 助教 (20532104)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 細胞バイオメカニクス / メカノバイオロジー / 細胞核 / DNA / メカノトランスダクション / 生体計測 / バイオメカニクス / 生体・情報計測 / 細胞骨格 |
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| Outline of Final Research Achievements |
We demonstrated the mechanical deformation and trapping of the intracellular nucleus using the microfabricated substrates. We investigated the effects of nuclear deformation on the physiological functions of cells. We found that the mechanical trapping of the cell nuclei with the micropillars significantly inhibited cell migration and DNA synthesis. The cell proliferation was significantly inhibited in the micropillar substrates even though the cells did not reach the confluent state. A detailed image analysis with confocal microscopy revealed that expression of lamin A/C was significantly decreased in the region deforming along the pillar surfaces, and underlying DNA distribution became more heterogeneous. These results may indicate that lamin A/C has a role of mechanosensor to detect an excessive deformation of nucleus, and they switch the cell state from an “active phase” to a“resting phase”.
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