2018 Fiscal Year Final Research Report
The establishment of a novel endometriosis model and the understanding of the developmental mechanism of endometriosis.
Project/Area Number |
16K11108
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Obstetrics and gynecology
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Research Institution | Keio University |
Principal Investigator |
MASUDA Hirotaka 慶應義塾大学, 医学部(信濃町), 講師 (80317198)
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Co-Investigator(Kenkyū-buntansha) |
丸山 哲夫 慶應義塾大学, 医学部(信濃町), 准教授 (10209702)
内田 浩 慶應義塾大学, 医学部(信濃町), 講師 (90286534)
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Keywords | 子宮内膜症 / 磁気ビーズ / モデルマウス / イメージングシステム / Bioluminescence imaging / 上皮間葉転換(EMT) |
Outline of Final Research Achievements |
We developed a non-invasive and real-time assessment system using in vivo bioluminescent imaging to quantitate human endometrium-derived cells transplanted in the murine peritoneal cavity, which demonstrate its possibility as a peritoneal endometriosis model. Human eutopic endometrial cells occurred EMT via EMT induction, while endometriotic epithelia showed a variety of EMT status according to a type of endometriosis. Therefore, EMT was thought to be involved in the establishment and the development of endometriosis. ZEB1 was likely to be expressed in endometriotic epithelia of invasive endometriosis, but not in eutopic endometrial epithelia. An EMT inhibitor could suppress adhesive capacity and motility of endometrial epithelial cells, indicating that the inhibitor could prevent the establishment and development of endometriosis. An EMT inhibitor can be a novel drug for endometriosis.
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Free Research Field |
生殖内分泌
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Academic Significance and Societal Importance of the Research Achievements |
子宮内膜症は不妊症に限らず、月経のある女性の6-10%に発症し、全世界で1.8 億人が月経困難や下腹部痛などによりQOL の低下を余儀なくされ、その経済的損失は患者・週あたり456 米ドル(Nnoaham et.al. FetilSteril. 2011)と算出されている。日本においても、年間約3800 億円の経済的損失(平成12 年度厚生科学研究報告書)があると計算されている。さらには、上皮性卵巣癌や腹膜癌の前癌病変とも考えられ、社会的にもインパクトの大きい疾患である。よって、子宮内膜症の解明や治療は、大きな社会的貢献につながると考えられる。
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