| Project/Area Number |
16K15456
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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 |
Respiratory organ internal medicine
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| Research Institution | Gunma University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
前野 敏孝 群馬大学, 医学部附属病院, 講師 (00436297)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 脂肪酸 / サーファクタント / 線維化 / 肺気腫 / 飽和脂肪酸 / 血管平滑筋 / 肺線維症 / 肺胞上皮細胞 / 肺線維化 / 肺胞上皮 |
|---|
| Outline of Final Research Achievements |
In the present study, we demonsrated that the lack of Elovl6 has a causative role in lung pathology. Apoptosis and ROS production were increased in Elovl6－/－ lung. Alveolar type II epithelial cells isolated from Elovl6－/－ mice and LA-4 cells produced increased levels of ROS. Elovl6 deficiency increased PA and decreased OA and PUFA content in alveolar type II epithelial cells both in vivo and in vitro. Expressions of the genes for FADS1, FADS2, FATPs and FAT/CD36 were significantly reduced in Elovl6－/－ mice, suggesting that cellular uptake of long-chain FAs, including PUFA, was impaired in Elovl6－/－ mice.
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