Development of a new treatment model for placental dysfunction
| Project/Area Number |
16K07091
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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 |
Laboratory animal science
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
ISOTANI Ayako 奈良先端科学技術大学院大学, 先端科学技術研究科, 准教授 (20444523)
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| Research Collaborator |
IKAWA masahito
YURI syunsuke
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 胎盤 / 不妊治療 / 動物モデル / 発生工学 / 実験動物 |
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| Outline of Final Research Achievements |
The placenta is an essential organ for supporting the growth of a fetus in the mother's body. Placental dysfunction causes repeated abortions and infertility. However, a method for the treatment of these conditions has not yet been established. In this study, Ets2 mutant mice were produced using genome editing technology, as a placental dysfunction model. A drug-inducible Cdx2-expressing embryonic stem (ES) cell line was established for use in the development of a new placental dysfunction treatment model. The ES cells were injected into an eight-cell embryo and made to express Cdx2 with the same timing as that of embryonic development. Although most of the ES-derived cells could not differentiate into trophoblasts, which are stem cells of the placenta, we observed that some of the Cdx2-expressed ES cells could differentiate into trophoblasts.
With further improvement, these results may provide a basis for establishing and developing a new placental dysfunction treatment model.
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| Academic Significance and Societal Importance of the Research Achievements |
胎盤機能不全モデルとして新に樹立したEts2変異マウスは、先行研究の表現型と異なる表現型を示した。遺伝型を比較解析することで表現型につながるEts2の分子生物学的な役割が明らかになっていくものと考えられる。薬剤誘導型Cdx2-ES細胞は、初期胚期の短時間でCdx2だけでは胎盤の元となる栄養芽細胞への分化は不十分であったが、一部、栄養芽細胞へ分化するものも認められた。さらなる工夫により、ES細胞が胎盤機能不全レスキューモデルに適用できる可能性が示唆された。
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Report
(4 results)
Research Products
(8 results)
