首页 | 本学科首页   官方微博 | 高级检索  
     


Differential Proteomic Analysis of Dimethylnitrosamine (DMN)‐Induced Liver Fibrosis
Authors:Xiujie Liu  Rongji Dai  Ming Ke  Imran Suheryani  Weiwei Meng  Yulin Deng
Affiliation:1. School of Life Science, Beijing Institute of Technology, Beijing, P. R. China;2. Beijing Key Laboratory for Separation and Analysis in Biomedicine and Pharmceuticals, Beijing Institute of Technology, Beijing, P. R. China
Abstract:Liver fibrosis is a common pathological feature of many chronic liver diseases. To characterize the entire panorama of proteome changes in dimethylnitrosamine (DMN)‐induced liver fibrosis, isobaric tags for relative and absolute quantitation (iTRAQ)‐based differential proteomic analysis is performed with DMN‐induced liver fibrosis rats. A total of 4155 confidently identified proteins are found, with 365 proteins showing significant changes (fold changes of >1.5 or < 0.67, p < 0.05). In metabolic activation, proteins assigned to drug metabolism enzymes (e.g., CYP2D1) change, suggesting that the liver protection mechanism is activated to relieve DMN toxicity. In addition, the altered proteins of immune response and oxidative stress may activate hepatic stellate cells. Glucose metabolism disorder in DMN model rats is demonstrated by a decrease in key enzymes (e.g., ACSL1) in fatty acid metabolism, a tricabolic acid cycle‐related enzyme (SDH), glycogenolysis enzyme, and gluconeogenesis enzymes (PC, PCKGC) and by an increase in glycolysis enzymes (e.g., HXK1). Meanwhile, alterations in iron and calcium ion homeostasis proteins are observed. Our results also show that mitochondrial dysfunction may be involved in DMN hepatotoxicity. In conclusion, these altered liver proteins in the DMN model and control rats provide data for understanding the functional mechanism of liver fibrosis.
Keywords:differential proteomics  dimethylnitrosamine  iTRAQ  liver fibrosis
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号