The effect of endometriosis on granulosa cells in follicle growth

2023 Fiscal Year Final Research Report

• Project/Area Number: 20K09615
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 56040:Obstetrics and gynecology-related
• Research Institution: Nagoya University
• Principal Investigator: Nakamura Tomoko 名古屋大学, 医学部附属病院, 准教授 (40732681)
• Co-Investigator(Kenkyū-buntansha): 岩瀬 明 群馬大学, 大学院医学系研究科, 教授 (20362246) ; 後藤 真紀 名古屋大学, 医学部附属病院, その他 (90378125) ; 大須賀 智子 名古屋大学, 医学系研究科, 准教授 (30778296)
• Project Period (FY): 2020-04-01 – 2024-03-31
• Keywords: 子宮内膜症 / 卵胞発育

Outline of Final Research Achievements

We reported that transcription factor 21 and periostin were involved in the regulation of fibrosis in endometriosis, and were both upregulated by inflammation (Ganieva U, 2020). We then developed a novel ovarian endometriosis mouse model and showed increased oxidative stress and repressed FSH receptor expression in granulosa cells (Hayashi S, 2020). We further evaluated follicular growth in this model with RNA-seq, IHC and tissue clearing. VEGF pathway expression was elevated, and angiogenesis was initiated at an abnormally early stage of follicle development. The number of early stage follicles were also significantly decreased in the ovaries with endometriomas, suggesting follicular depletion.

Free Research Field

子宮内膜症

Academic Significance and Societal Importance of the Research Achievements

子宮内膜症の治療薬は排卵を抑制するため、子宮内膜症合併不妊の女性は、内膜症治療か不妊治療かの二者択一を迫られている。本研究では、内膜症による卵胞発育障害の機序を、炎症と線維化、及び血管新生の観点から顆粒膜細胞障害から解明することで、排卵を抑制しない新規内膜症治療薬開発の一助となった。