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Comparative studies of early liver dysfunction in senescence-accelerated mouse using mitochondrial proteomics approaches
Liu, Yashu1; He, Jintang1; Ji, Shaoyi2,3; Wang, Qingsong1; Pu, Hai1; Jiang, Tingting1; Meng, Lingyao1; Yang, Xiuwei2,3; Ji, Jianguo1
刊名MOLECULAR & CELLULAR PROTEOMICS
2008-09-01
DOI10.1074/mcp.M800109-MCP200
7期:9页:1737-1747
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemical Research Methods
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]AGE-RELATED-CHANGES ; HEPATIC STEATOSIS ; 3-HYDROXY-3-METHYLGLUTARYL-COA SYNTHASE ; DIFFERENTIAL EXPRESSION ; ANIMAL-MODEL ; FATTY-ACIDS ; OXIDATION ; MICE ; BRAIN ; ALPHA
英文摘要

The liver is a complex and unique organ responsible for a breadth of functions crucial to sustaining life, especially for various metabolic processes in its mitochondria. Senescence-accelerated mouse prone/8 (SAMP8), a widely used aging model, exhibits an oxidative stress-induced aging phenotype and severe mitochondria-related liver pathology that are not seen in senescence-accelerated mouse resistant/1 (SAMR1). Here we used both two-dimensional electrophoresis- and ICAT-based mitochondrial proteomics analysis to view the liver mitochondrial protein alterations between SAMP8 and SAMR1. Compared with SAMR1, decreased expression and activity of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase were detected in SAMP8 at 6 months old (SAMP8-6m). As the key enzyme of ketogenesis, 3-hydroxy-3-methylglutaryl-CoA synthase is well known to be transcriptionally regulated by peroxisome proliferator-activated receptor alpha, which was also expressed at lower levels in SAMP8-6m livers. In addition, down-regulation of two peroxisome proliferator-activated receptor alpha target gene products (acyl-CoA oxidase and enoyl-CoA hydratase), elevation of triglyceride, and reduction of acetyl-CoA were observed, indicating abnormal fatty acid metabolism in SAMP8-6m livers. In addition eight proteins (NDUAA, NDUBA, NDUB7, NDUS1, NDUS3, NDUV1, ETFA, and UCRI) of mitochondrial complexes were down-regulated in SAMP8-6m, resulting in mitochondria-related liver dysfunction characterized by enhanced oxidative stress-induced molecular damage ( lipid peroxide and oxidized protein) and depressed energy production (ATP). Glutamine synthetase and ornithine aminotransferase involved in glutamine synthesis were up-regulated in SAMP8 livers at both 1 and 6 months old that may be related to the accumulation of glutamate and glutamine. Our work provided useful clues to understanding the molecular mechanism underlying liver dysfunction in senescence-accelerated mouse.

语种英语
WOS记录号WOS:000259154800011
引用统计
被引频次:35[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/59913
专题北京大学药学院
作者单位1.Peking Univ, Coll Life Sci, Natl Lab Prot Engn & Plant Genet Engn, Beijing 100871, Peoples R China
2.Peking Univ, Sch Pharmaceut Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100083, Peoples R China
3.Peking Univ, Sch Pharmaceut Sci, Dept Nat Med, Beijing 100083, Peoples R China
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GB/T 7714
Liu, Yashu,He, Jintang,Ji, Shaoyi,et al. Comparative studies of early liver dysfunction in senescence-accelerated mouse using mitochondrial proteomics approaches[J]. MOLECULAR & CELLULAR PROTEOMICS,2008,7(9):1737-1747.
APA Liu, Yashu.,He, Jintang.,Ji, Shaoyi.,Wang, Qingsong.,Pu, Hai.,...&Ji, Jianguo.(2008).Comparative studies of early liver dysfunction in senescence-accelerated mouse using mitochondrial proteomics approaches.MOLECULAR & CELLULAR PROTEOMICS,7(9),1737-1747.
MLA Liu, Yashu,et al."Comparative studies of early liver dysfunction in senescence-accelerated mouse using mitochondrial proteomics approaches".MOLECULAR & CELLULAR PROTEOMICS 7.9(2008):1737-1747.
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