Pigment Epithelium-Derived Factor Mediates Autophagy and Apoptosis in Myocardial Hypoxia/Reoxygenation Injury

doi:10.1371/journal.pone.0156059

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標題:	Pigment Epithelium-Derived Factor Mediates Autophagy and Apoptosis in Myocardial Hypoxia/Reoxygenation Injury
作者:	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
貢獻者:	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
關鍵字:	hypoxia-induced apoptosis ischemia/reperfusion injury h9c2 cells stress death pedf infarction cancer cardiomyocytes translocation
日期:	2016-05
上傳時間:	2018-01-18 11:37:39 (UTC+8)
出版者:	Public Library Science
摘要:	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.
關聯:	Plos One, v.11 n.5, e0156059
顯示於類別:	[通識教育中心] 期刊論文

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