Centre for Liver Research, School of Infection and Immunity, Institute of Biomedical Research, The Medical School, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
FEBS Lett. 2011 Mar 23;585(6):935-41. doi: 10.1016/j.febslet.2011.02.030. Epub 2011 Feb 25.
Hypoxia and hypoxia-reoxygenation (H-R) regulate human hepatocyte cell death by mediating the accumulation of reactive oxygen species (ROS). Hepatocytes within the liver are organised into peri-portal (PP) and peri-venous (PV) subpopulations. PP and PV hepatocytes differ in size and function. We investigated whether PP and PV human hepatocytes exhibit differential susceptibility to hypoxic stress. Isolated hepatocytes were used in an in vitro model of hypoxia and H-R. ROS production and cell death were assessed using flow cytometry. PV, and not PP hepatocytes, accumulate intracellular ROS in a mitochondrial dependent manner during hypoxia and H-R. This increased ROS regulates hepatocyte apoptosis and necrosis via a mitochondrial pathway. These findings have implications on the understanding of liver injury and application of potential therapeutic strategies.
缺氧和再氧合（H-R）通过调节活性氧（ROS）的积累来调节人肝细胞的死亡。肝脏中的肝细胞分为门脉周围（PP）和门脉周围（PV）亚群。PP 和 PV 肝细胞在大小和功能上存在差异。我们研究了 PP 和 PV 人肝细胞是否对缺氧应激表现出不同的敏感性。分离的肝细胞用于缺氧和 H-R 的体外模型。使用流式细胞术评估 ROS 产生和细胞死亡。在缺氧和 H-R 期间，PV 而不是 PP 肝细胞以依赖于线粒体的方式积累细胞内 ROS。这种增加的 ROS 通过线粒体途径调节肝细胞凋亡和坏死。这些发现对理解肝损伤和应用潜在的治疗策略具有重要意义。
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