2021 Fiscal Year Final Research Report
Elucidate the mechanism of LncRNA and aim to establish a treatment method for COPD of macrolides
| Project/Area Number |
19K17679
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53030:Respiratory medicine-related
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| Research Institution | Osaka City University |
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Principal Investigator |
IJIRI NAOKI 大阪市立大学, 大学院医学研究科, 病院講師 (10567788)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | COPD / NEAT1 / LncRNA / macrolides |
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| Outline of Final Research Achievements |
Therapies to control chronic airway inflammation, which is the main cause of COPD, have not been established, and the cause of inflammation is unknown. Therefore, we focused on NEAT1, which is a long non-coding RNA, and measured it by adding tobacco smoke extract using bronchial epithelial cells. As a result, NEAT1 increased and at the same time, inflammatory cytokines IL-6 and IL-8 also increased. When NEAT1 was inactivated, neither IL-6 nor IL-8 increased, suggesting a relationship with NEAT1. For macrolides, clarithromycin and azithromycin were used, but only the former increased Nrf2, which is a transcription factor that affects antioxidant activity.
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| Free Research Field |
COPD
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| Academic Significance and Societal Importance of the Research Achievements |
全身性炎症性疾患であるCOPDにおいては、抗酸化作用を示すNrf2の低下や、非COPDと比較して炎症性サイトカインが上昇していることも報告されている。しかしそれらの機序は現時点でも不明である。
そこで本研究では、炎症の惹起あるいは抑制といった作用があることが徐々に解明されつつあるLong non coding RNAの中でもNEAT1に注目し、COPDへの関与を示すことにより、今後のCOPD治療に対する新たな治療戦略に寄与するものである。
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