Mechanism of endometrial cell survival in the formation of endometriotic lesion
| Project/Area Number |
23590476
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 子宮内膜症 / 炎症 / 動物モデル / アンチトリプシン / マウスモデル / SERPINA1 / アンチトリプリン / 月経血 / モデルマウス / 出血 / インターロイキン6 / プロテアーゼ受容体 |
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| Research Abstract |
Endometriosis is the intractable disorder characterized by the presence of endometrial tissue outside of the uterine cavity. Distinct endometriosis-like lesions in our experimental internal bleeding mouse model exhibited the expression of high levels of inflammation factors. To identify changes in protein levels in endometriosis-like lesions, protein profile changes were compared with control (no bleeding) mice. Cell lysates from lesions from uOVX and control mice were analyzed by 2-D gel electrophoresis, followed by MALDI-TOF MS. The level of alpha1-antitrypsin (a1-AT) is decreased in lesions from mice that underwent uOVX. In cultured stromal cells, a1-AT inhibited the expression of inflammation and cell survival factors. Reduced a1-AT levels may exacerbate local inflammation, suggesting the possible involvement of a1-AT in the pathophysiology of endometriosis.
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Report
(4 results)
Research Products
(17 results)
