| Project/Area Number |
23592407
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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 |
Obstetrics and gynecology
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| Research Institution | Oita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NASU Kaei 大分大学, 医学部, 准教授 (30274757)
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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: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 子宮内膜症 / マイクロアレイ / エピジェネティクス / 増殖 / アポトーシス / 病態 / 薬物療法 |
|---|
| Research Abstract |
We identified histone deacetylase 1-target mRNAs that were up-regulated by valpronic acid (VPA) treatment in endometriotic cyst stromal cells (ECSCs) by an mRNA microarray technique. We chose CCAAT/enhancer-binding protein alfa (C/EBP alfa) for further functional experiments. C/EBP alfa expression was attenuated in ECSCs and in endometriotic tissues. The compulsory expression of C/EBA alfa directed the inhibition of cell proliferation and the induction of apoptosis in ECSCs. C/EBP alfa knockdown directed the stimulation of cell proliferation and the resistance to apoptosis in normal endometrial cells. The expressions of various growth- and apoptosis-related molecules were down-regulated by C/EBP alfa knockdown. Our findings suggest that an epigenetically suppressed tumor suppressor gene is involved in the pathogenesis of endometriosis by creating the proliferative, anti-apoptotic, and other disease-specific characteristics of endometriosis.
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