| Project/Area Number |
25860202
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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 |
General medical chemistry
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| Research Institution | Hirosaki University |
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Principal Investigator |
MARUYAMA Atsushi 弘前大学, 医学(系)研究科(研究院), 助教 (10431438)
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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: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ヘムオキシゲナーゼー１ / NRF2 / ノンコーディングRNA / 転写制御 / 酸化ストレス / ヘムオキシゲナーゼ / Nrf2 / エピジェネティクス |
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| Outline of Final Research Achievements |
Emerging evidence indicates that enhancer RNAs (eRNAs), which are long non-coding RNAs transcribed from gene enhancer regions, play important roles in the regulation of gene expression. However, it remains unknown whether eRNAs are involved in the human heme oxygenase-1 gene (HO-1) induction. HO-1 possesses two distantly located enhancers called E2 and E1 enhancers to regulate its transcription.
In this study, I demonstrated that eRNAs are transcribed from the human HO-1 enhancers. Focusing on E2-derived enhancer RNA (eRNA E2), I found eRNA E2 is induced in response to HO-1 substrate heme and oxidative stress-causing reagents such as diethyl maleate (DEM) in an NRF2-dependent manner. I also found DEM-induced HO-1 expression was selectively down-regulated by knockdown of the eRNA E2. Furthermore, DEM-induced Pol II binding to human HO-1 regions is attenuated in eRNA E2 knockdown cells. These results indicate that eRNA E2 is functional and required for the induction of HO-1.
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