Study on blockage of the IIF propagation for improvement endothelial vascular cell viability
| Project/Area Number |
25820063
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Thermal engineering
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| Research Institution | Kyushu University |
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Principal Investigator |
FUKUNAGA TAKANOBU 九州大学, 工学(系)研究科(研究院), 技術職員 (60591196)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 細胞内凍結 / ギャップ結合 / 細胞生存率 / 細胞内凍結の伝播 / ギャップ結合の可逆的阻害 |
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| Outline of Final Research Achievements |
Intracellular ice formation (IIF) propagates from cell to cell and causes lethal damage to the cell during the freezing process. In this study, we hypothesized that IIF passes through gap junctions between cells and that blockage of gap junctions increases cell viability after the freeze-thaw process because of the inhibited IIF propagation. Monolayer cultures of Madin-Darby canine kidney (MDCK) cells on glass coverslips were preincubated with and without the gap-junction blocker heptanol and subsequently frozen at different cooling rates on a temperature-controlled stage. Microscopic observations showed that IIF propagation was successfully inhibited in the blocked group. However, cell viability in the blocked group after thawing was significantly lower than that in the non-blocked group. Although results of this study did not confirm our hypotheses, they indicated the important role of gap-junctional communication in the occurrence of IIF and the consequent cell damage.
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Report
(3 results)
Research Products
(4 results)
