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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31004

    標題: Hypoxia Augments Increased HIF-1 alpha and Reduced Survival Protein p-Akt in Gelsolin (GSN)-Dependent Cardiomyoblast Cell Apoptosis
    作者: Yeh, Yu-Lan
    Ting, Wei-Jen
    Shen, Chia-Yao
    Hsu, Hsi-Hsien
    Chung, Li-Chin
    Tu, Chuan-Chou
    Chang, Sheng-Huang
    Day, Cecilia-Hsuan
    Tsai, Yuhsin
    Huang, Chih-Yang
    貢獻者: Changhua Christian Hosp, Dept Pathol
    Jen Teh Jr Coll Med Nursing & Management, Dept Med Technol
    China Med Univ & Hosp, Sch Chinese Med
    MeiHo Univ, Dept Nursing
    Mackay Mem Hosp, Div Colorectal Surg
    Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm, Tainan, Tainan County, Taiwan
    Armed Force Taichung Gen Hosp, Dept Internal Med, Div Chest Med
    Tsao Tun Psychiat Ctr, Dept Hlth
    China Med Univ, Sch Chinese Med
    Asia Univ, Dept Hlth & Nutr Biotechnol
    關鍵字: Gelsolin
    HIF-1 alpha
    Cardiomyoblast cell apoptosis
    日期: 2016-06
    上傳時間: 2018-01-18 11:39:38 (UTC+8)
    出版者: Humana Press Inc
    摘要: Cytoskeleton filaments play an important role in cellular functions such as maintaining cell shape, cell motility, intracellular transport, and cell division. Actin-binding proteins (ABPs) have numerous functions including regulation of actin filament nucleation, elongation, severing, capping, cross linking, and actin monomer sequestration. Gelsolin (GSN) is one of the actin-binding proteins. Gelsolin (GSN) is one of the actin-binding proteins that regulate cell morphology, differentiation, movement, and apoptosis. GSN also regulates cell morphology, differentiation, movement, and apoptosis. In this study, we have used H9c2 cardiomyoblast cell and H9c2-GSN stable clones to understand the roles and mechanisms of GSN overexpression in hypoxia-induced cardiomyoblast cell death. The data show that hypoxia or GSN overexpression induces HIF-1 alpha expression and reduces the expression of survival markers p-Akt and Bcl-2 in H9c2 cardiomyoblast cells. Under hypoxic conditions, GSN overexpression further reduces p-Akt expression and elevates total as well as cleaved GSN levels and HIF-1 alpha levels. In addition, GSN overexpression enhances apoptosis in cardiomyoblasts under hypoxia. Hypoxic challenge further induced activated caspase-3 and cell death that was attenuated after GSN knock down, which implies that GSN is a critical therapeutic target against hypoxia-induced cardiomyoblast cell death.
    關聯: Cell Biochemistry and Biophysics, v.74 n.2, pp.221-228
    Appears in Collections:[醫務管理系(所)] 期刊論文

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