Human endothelial senescence induced by IL-1α in vitro

作     者：YAO Aiyu 1,2 , ZHOU Jianjun 1, LIU Yabing 1, FENG Meifu 1* and ZHOU Rouli 2*(1. State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China 2. Department of Cell Biology and Medical Genetics, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100083, China) 

作者机构：StateKeyLaboratoryofBiomembraneandMembraneBiotechnologyInstituteofZoologyChineseAcademyofSciencesBeijing100080China DepartmentofCellBiologyandMedicalGeneticsSchoolofBasicMedicalSciencesHealthScienceCenterPekingUniversityBeijing100083China 

出 版 物：《Progress in Natural Science:Materials International》 (自然科学进展·国际材料(英文))

年 卷 期：2004年第3期

页      面：26-30+97页

学科分类：0710[理学-生物学] 07[理学] 071003[理学-生理学] 

主　　题：IL 1α endothelial cell senescence ROS antioxidant systems. 

摘      要：Interleukin 1 (IL 1) is an important proinflammatory cytokine that causes pleiotropic effects. Vascular endothelial cells stimulated by IL 1α can lead to the inflammatory response. Reactive oxygen species (ROS) are also generated at the site of inflammation and serve as an important factor against foreign invader. Here we report that long term stimulation of human vein endothelial cells with IL 1α can accelerate their senescence associated with β galactosidase activity. The flow cytometric analyses showed that most of the induced cells entered G 0 G 1 phase. DNA damage was more severe in senescent cells by comet assay. The induced cells by IL 1α had higher levels of ROS and malonyldialdehyde (MDA), lower activity of antioxidant enzymes and lower capacity of total antioxidant systems than control, which led to cell damage and cell degeneration, that is to say, which contributed to cellular senescence. Our results gave a direct proof to a new hypothesis—“the inflammation hypothesis of aging on cellular level, and also provided a basis for the study on anti aging and aging related diseases.