Receptor interacting protein 1 involved in ultraviolet B induced NIH3T3 cell apoptosis through expression of matrix metalloproteinases and reactive oxygen species production  

作　　者：YAN Yan LI Li XU Hao-xiang PENG Shi-guang, QU Tao WANG Bao-xi 

机构地区：[1]Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, China [2]Department of Dermatology, Beijing Chaoyang Hospital, CapitalMedical University, Beijing 100020, China [3]Institute of Dermatology, Chinese Academy of Medical Sciences andPeking Union Medical College, Nanjing, Jiangsu 210042, China

出　　处：《Chinese Medical Journal》2013年第22期4327-4333,共7页中华医学杂志（英文版）

基　　金：This work was supported by a grant from the National Natural Science Foundation of China （No. 81000702）. The authors have no conflicts of interest to declare.

摘　　要：Background Receptor interacting protein 1 （RIP1）, which plays a key role in apoptosis, cell survival and programmed cell necrosis, is one of the most important proteins in the RIP family. The purpose of this study was to investigate the roles of RIP1 in the apoptosis, the generation of reactive oxygen species （ROS） and the expression of matrix metalloproteinases （MMPs） induced by ultraviolet B （UVB） in fibroblasts. Methods siRNA targeting RIP1 was used to silence RIP1 expression in the NIH3T3 fibroblasts. The mRNA and protein levels of MMP-1 and MMP-3, caspase-3 and -8 activities, and ROS activities were determined by reverse transcriptasequantitative polymerase chain reaction （RT-qPCR）, immunoblotting, caspase activity assay, immunofiuorescence, and flow cytometry. Results The mRNA and protein expressions of MMP-1 and MMP-3 were significantly increased in RIP1 deficient NIH3T3 cells at 24 hours after UVB treatment. At 24 hours after exposure to UVB, RIP1 deficient NIH3T3 cells presented apoptotic morphology, and the apoptosis rate was significantly increased accompanied by pronounced increase in caspase-8 and -3 activities. ROS production was inhibited by UVB at 12 hours in RIP1 deficient NIH3T3 cells. Conclusion RIP1 is involved in NIH3T3 cell damage induced by UVB via participating in the apoptosis, expression of MMPs and ROS production.Background Receptor interacting protein 1 （RIP1）, which plays a key role in apoptosis, cell survival and programmed cell necrosis, is one of the most important proteins in the RIP family. The purpose of this study was to investigate the roles of RIP1 in the apoptosis, the generation of reactive oxygen species （ROS） and the expression of matrix metalloproteinases （MMPs） induced by ultraviolet B （UVB） in fibroblasts. Methods siRNA targeting RIP1 was used to silence RIP1 expression in the NIH3T3 fibroblasts. The mRNA and protein levels of MMP-1 and MMP-3, caspase-3 and -8 activities, and ROS activities were determined by reverse transcriptasequantitative polymerase chain reaction （RT-qPCR）, immunoblotting, caspase activity assay, immunofiuorescence, and flow cytometry. Results The mRNA and protein expressions of MMP-1 and MMP-3 were significantly increased in RIP1 deficient NIH3T3 cells at 24 hours after UVB treatment. At 24 hours after exposure to UVB, RIP1 deficient NIH3T3 cells presented apoptotic morphology, and the apoptosis rate was significantly increased accompanied by pronounced increase in caspase-8 and -3 activities. ROS production was inhibited by UVB at 12 hours in RIP1 deficient NIH3T3 cells. Conclusion RIP1 is involved in NIH3T3 cell damage induced by UVB via participating in the apoptosis, expression of MMPs and ROS production.

关 键 词：receptor interacting protein NIH3T3 ultraviolet B APOPTOSIS matrix metalloproteinase 

分 类 号：R363[医药卫生—病理学]