2016 Fiscal Year Final Research Report
Analysis of the pathogenesis of endometriosis focusing on intracellular communications.
| Project/Area Number |
26670725
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Research Collaborator |
Nakamura Koji
Sawada Ikuko
Yoshimura Akihiko
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 子宮内膜症 / エクソソーム / 腹膜中皮細胞 / CD44 / 細胞間情報伝達 |
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| Outline of Final Research Achievements |
The overcome of endometriosis is a critical issue to improve quality of life of women. As a pathogenesis, it is well accepted that endometriosis is a process produced by menstrual debris including endometrial tissue that escapes retrograde through fallopian tubes into pelvis. Thus, we hypothesized endometrial cells evolve to “endometriosis cells” during retrograde menstruation by receiving some information from cells located at fallopian tubes or peritoneal walls. Herein, we focused on exosomes produced from cells as an intracellular communication tool and intended to analyze the role of exosomes. As an initial step, exosomes were isolated from ovarian cancer cells. Exosomes were co-cultured with human peritoneal mesothelial cells (HPMCs) which internalized the exosomes. CD44, which was enriched in exosomes, transferred to HPMCs upon internalization, leading to high levels of CD44 in HPMCs membrane. We showed one possible role of exosomes as an intracellular communication tool.
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| Free Research Field |
婦人科腫瘍学
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