Molecular mechanisms of uterine luminal epithelium disappearance in the process of embryo implantation

2019 Fiscal Year Final Research Report

• Project/Area Number: 18K19601
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 56:Surgery related to the biological and sensory functions and related fields
• Research Institution: The University of Tokyo
• Principal Investigator: HIROTA YASUSHI 東京大学, 医学部附属病院, 准教授 (40598653)
• Co-Investigator(Kenkyū-buntansha): 藤田 知子 東京大学, 医学部附属病院, 特任研究員 (60375441)
• Project Period (FY): 2018-06-29 – 2020-03-31
• Keywords: 着床 / 子宮内膜 / 胚浸潤 / 管腔上皮 / 間質 / 低酸素誘導因子 / 細胞周期

Outline of Final Research Achievements

Although disappearance of the endometrial luminal epithelium occurs during the embryo invasion, the mechanism of this event has been unclear. We newly found that hypoxia inducible factor HIF2α and cell cycle suppressor RB1 have essential roles in embryo invasion. Stromal HIF2α acts on the detachment of the endometrial luminal epithelium from the stroma via hypoxia-related signals. RB1 suppresses cell proliferation of the endometrial luminal epithelium and induces the fragmentation of epithelial cells and its trophoblast phagocytosis at the embryo attachment site.

Free Research Field

生殖生物学、産婦人科学

Academic Significance and Societal Importance of the Research Achievements

本研究では胚浸潤の異常が起こる各種の遺伝子改変マウスを用いて、その異常の詳細を横断的に解析し、胚が子宮内膜に浸潤していく過程で起こる子宮内膜管腔上皮の消失のメカニズムを解析することを通して、胚浸潤という現象を分子細胞生物学的に理解することができた。ヒト着床障害の発症機序の解明につながる可能性があり、着床障害の診断・治療への応用が期待される。