In vivo study of the maternal envionment and delivery system.

2023 Fiscal Year Final Research Report

• Project/Area Number: 21H02387
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 42040:Laboratory animal science-related
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Kanai Masami 東京医科歯科大学, 統合研究機構, 教授 (70321883)
• Co-Investigator(Kenkyū-buntansha): 伊藤 日加瑠 香川大学, 医学部, 准教授 (50587392)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: 胎盤 / NRK / 分娩遅延

Outline of Final Research Achievements

The morphology of the placenta varies significantly among animal species. Primates, including humans, and rodents such as mice possess a hemomonochorial placenta, which has evolved similarly. In these placentas, the syncytiotrophoblast cells, which are in contact with maternal blood, are specialized for barrier functions and selective material exchange. The KO mice for the Nrk (NIK-related kinase) gene, which we originally isolated, exhibit placental hypertrophy and delayed parturition. From the phenotypes and RNA-seq analysis of these Nrk KO mice, we revealed that parturition is delayed because the rapid decline in maternal P4 (progesterone) levels typically observed at the onset of labor does not occur in Nrk KO individuals. Additionally, by investigating the candidate downstream genes of Nrk, we explored the switch mechanisms for signaling the transition from normal pregnancy to the onset of labor.

Free Research Field

実験動物学

Academic Significance and Societal Importance of the Research Achievements

NRK KOによって分娩遅延が引き起こされる。本研究から、マウス胎盤がヒト胎盤の疾患モデルとしてカウンターパートであること、NRKが分娩誘導因子である可能性を示す結果が得られた。今後、マウスNRKとその下位因子と、ヒト早産の共通因子を、in silicoと病理切片を用いて更に検索することで、将来、早産の原因探索が可能となり、治療につながる可能性が示唆された。