| Project/Area Number |
26460875
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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 |
Legal medicine
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| Research Institution | University of Fukui |
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Principal Investigator |
Shimada Ichiroh 福井大学, 学術研究院医学系部門, 教授 (20272908)
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| Co-Investigator(Kenkyū-buntansha) |
三好 憲雄 福井大学, 遠赤外領域開発研究センター, 客員教授 (40209961)
伊保 澄子 新潟大学, 医歯学総合研究科, 客員研究員 (80151653)
鈴木 史子 福井大学, 学術研究院医学系部門, 特命助教 (80291376)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 高濃度酸素曝露 / 瀰漫性肺胞傷害 / c-Myc / Bax / 肺サーファクタント蛋白 / カスパーゼ / 活性酸素種 / アポトーシス / NIH/3T3 細胞株 / A549 細胞株 |
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| Outline of Final Research Achievements |
Hyperoxia induced a decrease in SP-C/A expression in mouse lungs, and the SP-C downregulation was also confirmed in A549 cells. In addition to enhanced c-Myc expression, Bax expression also increased following mouse exposure to hyperoxia. In vitro analysis showed that expression of these genes was regulated in a cell-type-dependent manner, i.e., upregulation of c-Myc in NIH/3T3 cells and Bax in A549 cells occurred regardless of whether there was a similar decrease in cell viability and increase in caspase-3/7 activation in response to hyperoxia. ROS production and caspase-8 activation were also detected in both cells.
We concluded that hyperoxia induces ROS production and cell death in lung tissues through a cell-type specific mechanism involving upregulation of c-Myc/Bax, and caspase-8 and -3/7 activation-dependent pathways, thereby leading to the development of diffuse alveolar damage (DAD).
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