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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108218


    Title: Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis
    Authors: 林哲鈺;James C. Lin;Wei-Wen Kuo;Rathinasamy;Rathinasamy Baskaran;Ming-Cheng C;Ming-Cheng Chen;Tsung-Jung H;Tsung-Jung Ho;Ray-Jade Che;Ray-Jade Chen;Ya-Fanf Chen;Ya-Fanf Chen;Viswanadha V;Viswanadha Vijaya Padma;Ing-Shiow La;Ing-Shiow Lay;黃志揚;Chih-yang Huang
    Contributors: 生物科技學系
    Date: 2017-04
    Issue Date: 2017-10-30 10:44:18 (UTC+8)
    Abstract: Background:
    Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis.

    Methods:
    In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin.

    Results:
    The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression.
    Conclusions:
    Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure. (Cardiol J 2017; 24, 2: 195–205)
    Relation: Cardiology Journal
    Appears in Collections:[生物科技學系] 期刊論文

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