中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/23826
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 29490/55136 (53%)
Visitors : 2000066      Online Users : 525
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    CMUR > China Medical University Hospital > Jurnal articles >  Item 310903500/23826
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/23826


    Title: Estrogen Receptor-α and -β in Endometriosis and Normal Endometrium in Humans
    雌激素α與β接受體在子宮內膜異位症與正常子宮內膜組織之表現
    Authors: 林武周(Wu-Chou Lin);謝耀元(Yao-Yuan Hsieh);蔡輔仁(Fuu-Jen Tsai);張文正(Weng-Cheng Chang);張穎宜(Cherry Yin-Yi Chang);蔡鴻德(Horng-Der Tsai)
    Contributors: Department of Obstetrics and Gynecology, Department of Pediatrics and Medical Genetics, China Medical Univesity Hospital;School of Sports Medicine, China Medical University;Department of Biological Science and Technology, National Chiao Tung University
    Keywords: 子宮內膜異位;雌激素接受體;反轉錄聚合酶鏈反應;西方點漬法;endometriosis;estrogen receptor isoform;reverse transcription-polymerase chain reaction;Western blot analysis
    Date: 2005-06
    Issue Date: 2009-10-22
    Abstract: 目的 子宮內膜異位症之發生過程與雌激素有關,雌激素可經由α與β接受體結合作用引發進一步之生理作用機轉。本篇研究將計畫評估比較子宮內膜α與β接受體在子宮內膜異位症與正常子宮內膜組織之表現差異。方法 所有實驗材料區分爲三組:1)子宮內膜組織(取自子宮內膜異位症女性,n=11):2)子宮內膜異位瘤組織(取自子宮內膜異位症女性,n=11):3)子宮內膜組織(取自正常女性,n=10)。三組之雌激素α與β接受體之信使核糖酸(mRNA)以反轉錄聚合酶鏈反應(RT-PCR)進一步偵測,以西方點漬法(Western blotting)偵測其蛋白質表現,並進一步比較各組mRNA與蛋白質之表現差異。結果 各組雌激素α與β接受體之mRNA表現比例分別爲:1)31.9/60.61:2)0/76.23:3)67.15/89.48%。α接受體之表現於第一組表現最高,其次爲第二組,最低爲第三組。於各組中亦發現雌激素α之表現均比β接受體低。各組雌激素α與β接受體之蛋白質表現比例分別爲:1)47.21/60.52:2)37/48.21:3)45.45/61.77%。第一組與第二組之子宮內膜組織雌激素接受體蛋白質表現並無明顯差異。第三組子宮內膜異位瘤之激素體蛋白質明顯比第一組與第二組之蛋白質表現爲低。結論 雌激素β接受體之mRNA與蛋白質表現均比雌激素α接受體爲高,相對而言,於子宮內膜異位瘤之雌激素α接受體之mRNA與蛋白質表現明顯受到抑制。雌激素接受體之同型接受體基因可能與子宮內膜異位症之致病機轉有關。
    Purpose. Endometriosis is an estrogen-related disease. The biologic activity of estrogen is mediated by two high-affinity estrogen receptors, ER-α and ER-β. We aimed to evaluate the levels of expression of ER-α and -β in endometriotic lesions and normal endometrium. Methods. Samples were divided into three groups: Group 1 comprised eutopic endometrium from normal controls (n=10); Group 2 consisted of eutopic endometrium (n=11) and Group 3 ectopic endometrium (n=11) from endometriosis patients. ER-α and -β mRNA in each Group was surveyed with reverse transcriptase-polymerase chain reaction. Their protein levels were detected by Western blot analysis. ER-α and -β mRNA and protein expressions in each group were compared. Results The proportion of ER-α/-β mRNA expression was 67.15/89.48 in Group 3,31.9/60.61 in Group 1, and 0/76.23% in Group 2. ER-ct mRNA expression was highest in Group 1, moderate in Group 2, and lowest in Group 3 (p<0.05). ER-β mRNA expression was highest in Group 1, moderate in Group 3, and lowest in Group 2 (p<0.05). ER-α mRNA expression was significantly lower than ER-β mRNA in all groups. The proportion of ER-α/-β protein expression was 45.45/61.77 in Group 3, 47.21/60.52 in Group 1, and 37/48.21% in Group 2. ER protein expression in eutopic endometrium in Groups 3 and 1 did not differ significantly. ER protein expression in ectopic endometrium was significantly lower than in eutopic endometrium in Groups 3 and 1. Conclusions. ER-β protein expression is higher than ER-α in normal endometrium and in endometritic tissue. ER-α mRNA and protein are suppressed in endometriotic tissue. The ER gene isoforms likely contribute to the pathogenesis of endometriosis.
    Relation: Mid-Taiwan Journal of Medicine 10(2):65-72
    Appears in Collections:[台中附設醫院] 期刊論文

    Files in This Item:

    File SizeFormat
    2005066572.pdf307KbAdobe PDF617View/Open


    All items in CMUR are protected by copyright, with all rights reserved.

     


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback