Cell and molecular mechanismas of placental syncytialisation: pathogenesis of preeclampsia

2020 Fiscal Year Final Research Report

• Project/Area Number: 17K11238
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Hiroshima University
• Principal Investigator: KUDO Yoshiki 広島大学, 医系科学研究科(医), 教授 (80241082)
• Co-Investigator(Kenkyū-buntansha): 古宇 家正 広島大学, 病院(医), 講師 (10794779)
• Project Period (FY): 2017-04-01 – 2021-03-31
• Keywords: 胎盤 / トロフォブラスト / シンシチウム化 / 妊娠高血圧症候群 / 癒着胎盤

Outline of Final Research Achievements

1. The expression of syncytin, a molecule that promotes syncytialisation of human placental trophoblast, suppressyn, a molecule that suppresses syncytialisation, and ASCT2, a receptor for them, was analysed in the placenta of preeclampsia. As a result, enhanced expression of suppressyn was observed in the placenta of preeclampsia as compared with the placenta of normal pregnancy.
2. The expression kinetics of indoleamine 2,3-dioxygenase (IDO), a tryptophan-catabolising enzyme, was analysed at the maternal-fetal interface of human pregnancy. It was suggested that the invasion of trophoblast was controlled by IDO, and that no expression of IDO was observed in the decidua of placenta accreta, which could be the pathogenesis of this pathological pregnancy.

Free Research Field

産婦人科学

Academic Significance and Societal Importance of the Research Achievements

妊娠高血圧症候群は周産期医療の発達した現在においても高頻度かつ母児共に生命に危険のある重篤な妊娠合併症である。その発症には胎盤の関与が示唆されており、病理組織学的にシンシチオトロフォブラストの形成不全が認められるのが特徴である。この研究で得られた結果は、シンシチオトロフォブラスト形成の調節機構、さらには妊娠高血圧症候群およびそれに合併する子宮内胎児発育不全の発症病態の分子生物学的機序の解明につながると考えられる。