中国科学院大连化学物理研究所机构知识库
Advanced  
DICP OpenIR  > 中国科学院大连化学物理研究所  > 期刊论文
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 ;  Life Sciences & Biomedicine
类目[WOS]: Biochemical Research Methods ;  Biochemistry & Molecular Biology
研究领域[WOS]: Biochemistry & Molecular Biology
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.
关键词[WOS]: UT-B ;  OXIDATIVE STRESS ;  CONCENTRATING ABILITY ;  HEART-FAILURE ;  CYTOCHROME-C ;  PROTEIN ;  HSP60 ;  APOPTOSIS ;  ERYTHROCYTES ;  MUTATION
语种: 英语
WOS记录号: WOS:000342912600015
Citation statistics: 
内容类型: 期刊论文
URI标识: http://cas-ir.dicp.ac.cn/handle/321008/143194
Appears in Collections:中国科学院大连化学物理研究所_期刊论文

Files in This Item:

There are no files associated with this item.


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.
Service
 Recommend this item
 Sava as my favorate item
 Show this item's statistics
 Export Endnote File
Google Scholar
 Similar articles in Google Scholar
 [Du, Yanwei]'s Articles
 [Meng, Yan]'s Articles
 [Zhu, Jun]'s Articles
CSDL cross search
 Similar articles in CSDL Cross Search
 [Du, Yanwei]‘s Articles
 [Meng, Yan]‘s Articles
 [Zhu, Jun]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
  Add to CiteULike  Add to Connotea  Add to Del.icio.us  Add to Digg  Add to Reddit 
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Powered by CSpace