| Project/Area Number |
16K20200
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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 |
Obstetrics and gynecology
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| Research Institution | Oita University |
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Principal Investigator |
KAI Kentaro 大分大学, 医学部, 客員研究員 (90457622)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 子宮内膜症 / マイクロRNA / 脱落膜化 / ジエノゲスト / エピジェネティクス / ネットワーク解析 / マイクロアレイ / プロゲスチン / 子宮内膜 / インスリン様成長因子 / プロラクチン / Prolactin / IGFBP1 / miRNA |
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| Outline of Final Research Achievements |
The objective of this study is to elucidate the molecular pathways of decidualization in eutopic and ectopic endometrium. We isolated normal endometrial stromal cells (NESCs) and endometriotic cyst stromal cells (ECSCs) and cultured them with dibutyryl cyclic-AMP and dienogest for 12 days. We analyzed the expression patterns of microRNA (miRNA) and mRNA by microarray and an ingenuity pathway analysis. Enhanced expression of miR-30 family members was observed in both decidualized NESCs and decidualized ECSCs, whereas miR-210 was upregulated in decidualized ECSCs only. We found three candidate pathways involved in the decidualization. Our results revealed that aberrantly expressed miRNA is involved in decidualization. We suggested that the miR-30 family members are novel signaling molecules conserved in both NESCs and ECSCs, and that the miR-210 family is conserved in only ECSCs.
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