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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/29563


    標題: Neonatal Death and Heart Failure in Mouse with Transgenic HSP60 Expression
    作者: Chen, Tsung-Hsien
    Liu, Shan-Wen
    Chen, Mei-Ru
    Cho, Kuan-Hung
    Chen, Tzu-Yin
    Chu, Pao-Hsien
    Kao, Yu-Ying
    Hsu, Ching-Han
    Lin, Kurt Ming-Chao
    貢獻者: 生物科技系
    關鍵字: Shock proteins
    Molecular chaperones
    Ischemia/reperfusion injury
    Apoptosis
    Heat-shock-protein-60
    Stress
    Cells
    Hsp10
    Mice
    Overexpression
    日期: 2015
    上傳時間: 2016-04-19 19:00:23 (UTC+8)
    出版者: Hindawi Publishing Corp
    摘要: Mitochondrial heat shock proteins, such as HSP60, are chaperones responsible for the folding, transport, and quality control of mitochondrial matrix proteins and are essential for maintaining life. Both prosurvival and proapoptotic roles have been proposed for HSP60, and HSP60 is reportedly involved in the initiation of autoimmune, metabolic, and cardiovascular diseases. The role of HSP60 in pathogenesis of these diseases remains unclear, partly because of the lack of mouse models expressing HSP60. In this study we generated HSP60 conditional transgenic mice suitable for investigating in vivo outcomes by expressing HSP60 at the targeted organ in disease models. Ubiquitous HSP60 induction in the embryonic stage caused neonatal death in mice at postnatal day 1. A high incidence of atrial septal defects was observed in HSP60-expressing mice, with increased apoptosis and myocyte degeneration that possibly contributed to massive hemorrhage and sponge-like cardiac muscles. Our results showed that neonatal heart failure through HSP60 induction likely involves developmental defects and excessive apoptosis. The conditional HSP60 mouse model is useful for studying crucial biological questions concerning HSP60.
    Appears in Collections:[生物科技系(所)] 期刊論文

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