| Project/Area Number |
26461678
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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 |
Dermatology
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
伊藤 由美子 東北大学, 大学病院, 臨床検査技師 (00375057)
相場 節也 東北大学, 医学系研究科, 教授 (80159269)
木村 裕 東北大学, 大学病院, 助教 (90375056)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | heme oxygenase-1 / ferroportin / 表皮細胞 / HO-1 / hemeoxygenase-1 (HO-1) / RAG2KOマウス / common gamma鎖KOマウス / ILC1 / ILC2 / アレルギー性接触性皮膚炎 / RAG2ノックアウトマウス / NK cell |
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| Outline of Final Research Achievements |
We have been studying the role of heme oxygenase-1 (HO-1) in the epidermis. At the same time, we investigated the expression of ferroportin (Fpn), an iron transport membrane protein, in the murine epidermis and discovered that Fpn expression was induced as epithelial cells (EC) differentiate, which was correlated with HO-1 expression. To further investigate the role of both molecules in the epidermis, we created EC-specific HO-1-deficient mice and EC-specific Fpn-deficient mice. In the EC-specific HO-1-deficient mice, we found that the mice developed not only skin inflammation in the steady state but also weight loss. In the EC-specific Fpn-deficient mice gradually suffered from anemia. These results indicated that these two molecules affected the whole body condition as well as the epidermis. Further examination on the molecular basis of cooperation between these two molecules will provide the mechanism by which the skin metabolism affects the whole body metabolism.
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