| Project/Area Number |
24659731
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Tottori University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IZAWA Masao 鳥取大学, 医学部, 特任教授 (50032222)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 子宮内膜症 / アロマターゼ遺伝子 / 高エストロゲン環境 / エストロゲン受容体バリアント発現 / エストロゲン受容体バリアント / 組織特異的プロモーター活性 / 選択的翻訳 / エストロゲン受容体発現 |
|---|
| Research Abstract |
A maked up-regulation of aromatase gene leads to a hight estrogen environment in endometriotic tissues. The urgent issue to be clarified is to understand the molecular basis of estrogen action. So far, a higher estrogen reseptor (ER) beta and a lower ER alpha endometriotic tissues have been documented to explain the pathophysiology of endometriosis.
We re-evaluated the molecular basis of ER expression in endometriotic tissues. Transcripts for 4 ER beta variants were detectable. Among them, the ER beta 5 was the most dominant. ER alpha mRNA the expression in endometriotic cells was 7-fold lower than that in endometrial cells. Although a single cDNA sequence predicting a wild-type 66KDa ER alpha was detectable, the protein expression was found to be a 55KDa molecule.
Findings provide a new facet in understanding the pathophysiological role of high estrogen in endometriosis.
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