| Project/Area Number |
17K10186
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
Hayato Go 福島県立医科大学, 医学部, 講師 (30443857)
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| Co-Investigator(Kenkyū-buntansha) |
桃井 伸緒 福島県立医科大学, 医学部, 教授 (10285033)
橋本 浩一 福島県立医科大学, 医学部, 准教授 (50322342)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 新生児慢性肺疾患 / Extracellular vesicles / Exosome / microRNA / miR-21 / エクソソーム / 慢性肺疾患 / miRNA |
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| Outline of Final Research Achievements |
Serum EVs were extracted from premature infants at birth and on the 28th day of life (DOL). Using a human miRNA array, we identified 62 miRNAs that were universally expressed in CLD patients and non-CLD patients. Of these miRNAs, serum EV miR-21 was upregulated in CLD patients on DOL28 compared with levels at birth and downregulated in non-CLD patients on DOL28 compared with levels at birth. . We conclude that EV miR-21 may be a biomarker of CLD. In CLD mouse model exposed to hyperoxia, pulmonary function in mice after injection of miR-21 inhibitor was improved. This suggests that miR-21 could be a potential therapeutic target for CLD.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、miR-21が新生児慢性肺疾患のバイオマーカーになり得ることを示し、さらに動物実験ではmiR-21を制御することでCLDマウスの呼吸機能が改善していたため、miR-21が新生児慢性肺疾患の治療標的となり得る可能性が示唆された。
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