Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/30905
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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/30905


    Title: Pigment Epithelium-Derived Factor Mediates Autophagy and Apoptosis in Myocardial Hypoxia/Reoxygenation Injury
    Authors: Kuo, Hsuan-Fu
    Liu, Po-Len
    Chong, Inn-Wen
    Liu, Yu-Peng
    Chen, Yung-Hsiang
    Ku, Po-Ming
    Li, Chia-Yang
    Chen, Hsiu-Hua
    Chiang, Hui-Ching
    Wang, Chiao-Lin
    Chen, Huang-Jen
    Chen, Yen-Chieh
    Hsieh, Chong-Chao
    Contributors: Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Kaohsiung Municipal Ta Tung Hosp, Dept Internal Med
    Kaohsiung Med Univ, Coll Med, Dept Resp Therapy
    Kaohsiung Med Univ, Dept Genome Med
    China Med Univ, Coll Chinese Med, Grad Inst Integrated Med
    Asia Univ, Coll Med & Hlth Sci, Dept Psychol
    Chi Mei Hosp, Cardiovasc Ctr
    Chia Nan Univ Pharm & Sci
    Kaohsiung Med Univ Hosp, Dept Surg, Div Cardiovasc Surg
    Keywords: hypoxia-induced apoptosis
    ischemia/reperfusion injury
    h9c2 cells
    stress
    death
    pedf
    infarction
    cancer
    cardiomyocytes
    translocation
    Date: 2016-05
    Issue Date: 2018-01-18 11:37:39 (UTC+8)
    Publisher: Public Library Science
    Abstract: Pigment epithelium-derived factor (PEDF) is a multifunctional protein that exhibits antiangiogenic, antitumor, anti-inflammatory, antioxidative, anti-atherogenic, and cardioprotective properties. While it was recently shown that PEDF expression is inhibited under low oxygen conditions, the functional role of PEDF in response to hypoxia/reoxygenation (H/R) remains unclear. The goal of this study was to therefore investigate the influence of PEDF on myocardial H/R injury. For these analyses, PEDF-specific small interfering RNA-expressing and PEDF-expressing lentivirus (PEDF-LV) vectors were utilized to knockdown or stably overexpress PEDF, respectively, within human cardiomyocytes (HCM) in vitro. We noted that reactive oxygen species (ROS) play important roles in the induction of cell death pathways, including apoptosis and autophagy in ischemic hearts. Our findings demonstrate that overexpression of PEDF resulted in a significant reduction in ROS production and attenuation of mitochondrial membrane potential depletion under H/R conditions. Furthermore, PEDF inhibited the activation of a two-step apoptotic pathway in which caspase-dependent (caspase-9 and caspase-3) and caspase-independent (apoptosis inducing factor and endonuclease G), which in turn cleaves several crucial substrates including the DNA repair enzyme poly (ADP-ribose) polymerase. Meanwhile, overexpression of PEDF also promoted autophagy, a process that is typically activated in response to H/R. Therefore, these findings suggest that PEDF plays a critical role in preventing H/R injury by modulating anti-oxidant and anti-apoptotic factors and promoting autophagy.
    Relation: Plos One, v.11 n.5, e0156059
    Appears in Collections:[The Center For General Education] Periodical Articles

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