The mitochondrial function was impaired in APP knockout mouse embryo fibroblast cells  

作　　者：SHENG BaiYang NIU Ying ZHOU Hui ZHOU Hui YAN JiaXin ZHAO NanMing ZHANG XiuFang GONG YanDao 

机构地区：[1]State Key Laboratory of Biomembrane and Membrane Biotechnology, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, China [2]Wuhan Institute of-Biological Products, Wuhan 430060, China [3]Medical School, Tsinghua University, Beijing 100084, China

出　　处：《Chinese Science Bulletin》2009年第10期1725-1731,共7页

基　　金：Supported by Tsinghua-Yue-Yuen Medical Sciences Fund (Grant No. 20240000514);Science and Technology Planning Project of Beijing Municipal (Grant No. H060920050430);State Key Laboratory of Biomembrane and Membrane Bio-technology

摘　　要：The amyloid precursor protein (APP) is recognized as the source of Aβ, which plays an important role in Alzheimer’s disease. However, the biological function of APP is obscure. Previous studies showed that mitochondria could be a target of APP. In this work, APP knockout mouse embryo fibroblast (MEF) cells were used to test if APP plays any role in maintaining the mitochondrial function. As the result, APP knockout MEF cells (APP-/- cells) showed the abnormal mitochondrial function, including slower cell proliferation, lower mitochondrial membrane potential, lower intracellular ROS, higher mitochondrial membrane fluidity and lower cytochrome c oxidase activity than their wild-type counterparts. However, no change was found in the amount of mitochondria in MEF APP-/-cells.The amyloid precursor protein （APP） is recognized as the source of Aβ, which plays an important role in Alzheimer＇s disease. However, the biological function of APP is obscure. Previous studies showed that mitochondria could be a target of APP. In this work, APP knockout mouse embryo fibroblast （MEF） cells were used to test if APP plays any role in maintaining the mitochondrial function. As the result, APP knockout MEF cells （APP-/- cells） showed the abnormal mitochondrial function, including slower cell proliferation, lower mitochondrial membrane potential, lower intracellular ROS, higher mitochondrial membrane fluidity and lower cytochrome c oxidase activity than their wild-type counterparts. However, no change was found in the amount of mitochondria in MEF APP-/- cells.

关 键 词：胚胎成纤维细胞 线粒体膜电位 亚洲 功能障碍 小鼠 细胞色素C氧化酶 阿尔茨海默氏病 应用程序 

分 类 号：Q959.837[生物学—动物学] S865.13[农业科学—野生动物驯养]