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学科主题: 基础医学
题名:
Quantitative proteomic study of myocardial mitochondria in urea transporter B knockout mice
作者: Du, Yanwei1; Meng, Yan1; Zhu, Jun2; Kang, Le1; Jia, Xiaolong1; Guo, Lirong1; Zhang, Ling1; Ye, Mingliang2; Hu, Lianghai3; Zhao, Xuejian1; Gu, Jingkai3; Yang, Baoxue1,4; Zou, Hanfa2
关键词: Animal proteomics ; Heart ; Mitochondria ; Urea transporter
刊名: PROTEOMICS
发表日期: 2014-09-01
DOI: 10.1002/pmic.201400123
卷: 14, 期:17-18, 页:2072-2083
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemical Research Methods ; Biochemistry & Molecular Biology
研究领域[WOS]: Biochemistry & Molecular Biology
关键词[WOS]: UT-B ; OXIDATIVE STRESS ; CONCENTRATING ABILITY ; HEART-FAILURE ; CYTOCHROME-C ; PROTEIN ; HSP60 ; APOPTOSIS ; ERYTHROCYTES ; MUTATION
英文摘要:

In previous research, we showed that 16-week-old urea transporter B (UT-B) null mice have an atrial-ventricular conduction block, and hypothesized myocardial mitochondrial dysfunction. To investigate the mechanism of this block, we examined the proteomic differences in the myocardial mitochondria of UT-B null and wild-type mice with nanoscale LC-MS/MS. Of 26 proteins clearly downregulated in the UT-B null mice, 15 are involved in complexes I, III, IV, and V of the respiratory chain, which would strongly reduce the activity of the electron transport chain. Excess electrons from complexes I and III pass directly to O-2 to generate ROS and deplete ROS-scavenging enzymes. Myocardial intracellular ROS were significantly higher in UT-B null mice than in wild-type mice (p < 0.01), constituting an important cause of oxidative stress injury in the myocardia of UT-B null mice. The mitochondrial membrane potential (Delta Psi m) was also lower in UT-B null mice than in wild-type mice (p < 0.05), causing oxidative phosphorylation dysfunction of complex V and insufficient ATP in the myocardial cells of UT-B null mice. HADHA (a trifunctional protein) and HSP60 were also downregulated in the UT-B null myocardial mitochondria. These results confirm that mitochondrial dysfunction underlies the pathogenesis of the atrial-ventricular conduction block in UT-B null mice.

语种: 英语
所属项目编号: 81170304 ; 21105036 ; 81000271 ; 30900518 ; 81373374 ; NCET-12-0234
项目资助者: National Natural Science Foundation of China ; Program for New Century Excellent Talents in University
WOS记录号: WOS:000342912600015
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57326
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Jilin Univ, Coll Basic Med, Minist Educ, Key Lab Pathobiol,Dept Pathophysiol, Changchun 130021, Peoples R China
2.Chinese Acad Sci, Dalian Inst Chem Phys, CAS Key Lab Separat Sci Analyt Chem, Dalian, Peoples R China
3.Jilin Univ, Sch Life Sci, Minist Educ, Key Lab Mol Enzymol & Engn, Changchun 130021, Peoples R China
4.Peking Univ, Sch Basic Med Sci, Dept Pharmacol,Minist Educ, Key Lab Nat & Biomimet Drugs,Key Lab Mol Cardiova, Beijing 100871, Peoples R China

Recommended Citation:
Du, Yanwei,Meng, Yan,Zhu, Jun,et al. Quantitative proteomic study of myocardial mitochondria in urea transporter B knockout mice[J]. PROTEOMICS,2014,14(17-18):2072-2083.
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