Investigation for pathogenesis of endometriosis with a novel onset model

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K18674
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 56040:Obstetrics and gynecology-related
• Research Institution: Sapporo Medical University
• Principal Investigator: Shimada Hiroshi 札幌医科大学, 医学部, 訪問研究員 (00838906)
• Project Period (FY): 2019-04-01 – 2021-03-31
• Keywords: 子宮内膜症 / タイト結合 / LSR/angulin-1 / Cingulin

Outline of Final Research Achievements

We investigated for pathogenesis of endometriosis focusing on tight junction protein, LSR/angulin-1 and cellular signal transduction related to progression of endometriosis. In results, we reported that LSR/angulin-1 was responsible for cellular barrier, migration and division in normal endometrial epithelial cells. Moreover, we found that one of tight junction protein, Cingulin was responsible for cellular division in normal endometrial epithelial cells.

Free Research Field

細胞科学、生殖内分泌治療学

Academic Significance and Societal Importance of the Research Achievements

子宮内膜症は全女性の10％の有病率であり、月経痛や不妊症の原因となっている。一方で治療方法は一部の内服治療や手術療法のみと限られており、新規治療開発が求められている。本研究は正常子宮内膜細胞を用いることで、子宮内膜症発症のメカニズムを解明し、将来的に子宮内膜症発症予防の治療につながる重要な研究と考えられる。