| Project/Area Number |
15K10679
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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 |
Obstetrics and gynecology
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| Research Institution | Oita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
平川 東望子 大分大学, 医学部, 助教 (20516132)
奈須 家栄 大分大学, 医学部, 教授 (30274757)
河野 康志 大分大学, 医学部, 准教授 (40274758)
甲斐 健太郎 大分大学, 医学部, 助教 (90457622)
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| Project Period (FY) |
2015-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 子宮内膜症 / マイクロRNA / エピジェネティクス / miR-210 / STAT3 / 病態 / microRNA / VEGF / 細胞増殖 / アポトーシス |
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| Outline of Final Research Achievements |
We investigate the roles of the microRNA miR-210, a miRNA that is upregulated in endometriotic cyst stromal cells (ECSCs), in the pathogenesis of endometriosis.
We used a global gene expression microarray technique to identify downstream targets of miR-210, and we assessed compulsory miRNA expression in normal endometrial stromal cells (NESCs) to determine the functions of miR-210 in endometriosis. We found that miR-210 transfection into NESCs resulted in the induction of cell proliferation, the production of vascular endothelial cell growth factor, and the inhibition of apoptosis through signal transducer and activator of transcription (STAT) 3 activation. The results indicate that miR-210 induces NESCs to differentiate into the endometriotic phenotype, which is characterized by angiogenic, proliferative, and anti-apoptotic features.
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| Academic Significance and Societal Importance of the Research Achievements |
子宮内膜症の原因解明を目的として、マイクロRNAの発現以上に着目し、エピジェネティクスの観点から検討を行った。本研究では、卵巣子宮内膜症性嚢胞間質細胞において発現が亢進しているmiR-210 について、miR-210 の強制発現により制御される標的遺伝子としてsignal transducer and activator of transcription (STAT) 3を同定した。STAT3は子宮内膜症の病態形成に関与することが明らかとなった。
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