title: Reactive oxygen species contribute to simulated ischemia/reperfusion-induced autophagic cell death in human umbilical vein endothelial cells.
abstract: BACKGROUND
  Autophagy is important for cells to degrade protein aggregates and organelles. Our preliminary study suggests that ischemia/reperfusion in rabbit hearts promoted autophagic myocardial injury, resulting in no-reflow phenomenon. In this study, we sought to further understand the mechanism and outcome of the upregulation of autophagy in ischemia/reperfusion.
  
  
  METHODS
  We employed a simulated ischemia/reperfusion (sI/R) model in human umbilical vein endothelial cells (HUVECs) in vitro, in the presence or absence of antioxidants.
  
  
  RESULTS
  Our study confirms that sI/R induces autophagy in HUVECs as measured by increased expression of Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3), electron microscopic analysis, and special biofluorescent staining with monodansylcadaverine. This sI/R-induced autophagy was also accompanied by increased levels of p65 protein expression and cell death. In addition, we detected the accumulation of reactive oxygen species (ROS) after sI/R. Moreover, with the application of ROS scavengers that block the release of ROS, we were able to demonstrate that inhibition of autophagy increases cell survival.
  
  
  CONCLUSIONS
  The study suggests that ROS accumulation is involved in the sI/R-induced autophagic cell death in HUVECs.
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Min
authors.initials: M
authors.lastname: Zeng
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Xin
authors.initials: X
authors.lastname: Wei
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Zhiyong
authors.initials: Z
authors.lastname: Wu
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Bing
authors.initials: B
authors.lastname: Li
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Yi
authors.initials: Y
authors.lastname: Fei
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Yangli
authors.initials: Y
authors.lastname: He
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Jixiong
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
authors.affiliation: Department of Cardiology, People's Hospital of Hainan Province, Haikou, China (mainland).
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Liu
mesh_terms: D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001343:Autophagy; D000071186:Beclin-1; D002470:Cell Survival; D016166:Free Radical Scavengers / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D006801:Humans; D007511:Ischemia / Q000473:pathology*; D008565:Membrane Proteins / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000473:pathology*; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; C491997:BECN1 protein, human; D000071186:Beclin-1; D016166:Free Radical Scavengers; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins; D017382:Reactive Oxygen Species; D051996:Transcription Factor RelA