Investigate the adhesion molecules that control the progression of endometriosis.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462592
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Osaka University
• Principal Investigator: Hashimoto Kae 大阪大学, 医学(系)研究科(研究院), 助教 (90612078)
• Co-Investigator(Kenkyū-buntansha): Sawada Kenjiro 大阪大学, 医学系研究科, 講師 (00452392) ; Mabuchi Seiji 大阪大学, 医学系研究科, 助教 (00452441) ; Isobe Aki 大阪大学, 医学系研究科, 助教 (60397619)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 子宮内膜症 / 接着因子

Outline of Final Research Achievements

iTRAQ-based proteomics demonstrated that VCAM-1 was one of the increased membrane proteins of endometrial stromal cell of ovarian endometrial cyst (eESC) in comparison of normal eutopic endometrial stromal cells. Immunohistochemistry of endometriotic cyst and normal uterus showed comparative result. At eESC, VCAM-1 was regulated by nuclear factor kappa B (NF-κB). Adhesion of endometrial cell to peritoneal wall is one of the favored mechanisms of arising endometriosis. VCAM-1 neutralizing antibody and IKK inhibitor, which inhibits NF-κB activation, decreased adhesive activity of eESC to human peritoneal mesothelial cells (HPMC). In conclusion, VCAM-1 is the novel therapeutic target of endometriosis, and VCAM-1 neutralizing antibody and IKK inhibitor is potent therapeutic drug of endometriosis.

Free Research Field

医歯薬学