DICP OpenIR
Quantitative proteomic study of myocardial mitochondria in urea transporter B knockout mice
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
KeywordAnimal Proteomics Heart Mitochondria Urea Transporter
Source PublicationPROTEOMICS
2014-09-01
DOI10.1002/pmic.201400123
Volume14Issue:17-18Pages:2072-2083
Indexed BySCI
SubtypeArticle
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
WOS SubjectBiochemical Research Methods ; Biochemistry & Molecular Biology
WOS Research AreaBiochemistry & Molecular Biology
WOS KeywordUT-B ; OXIDATIVE STRESS ; CONCENTRATING ABILITY ; HEART-FAILURE ; CYTOCHROME-C ; PROTEIN ; HSP60 ; APOPTOSIS ; ERYTHROCYTES ; MUTATION
AbstractIn 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.
Language英语
WOS IDWOS:000342912600015
Citation statistics
Cited Times:5[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://cas-ir.dicp.ac.cn/handle/321008/143194
Collection中国科学院大连化学物理研究所
Affiliation1.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
GB/T 7714
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.
APA Du, Yanwei.,Meng, Yan.,Zhu, Jun.,Kang, Le.,Jia, Xiaolong.,...&Zou, Hanfa.(2014).Quantitative proteomic study of myocardial mitochondria in urea transporter B knockout mice.PROTEOMICS,14(17-18),2072-2083.
MLA Du, Yanwei,et al."Quantitative proteomic study of myocardial mitochondria in urea transporter B knockout mice".PROTEOMICS 14.17-18(2014):2072-2083.
Files in This Item:
There are no files associated with this item.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Du, Yanwei]'s Articles
[Meng, Yan]'s Articles
[Zhu, Jun]'s Articles
Baidu academic
Similar articles in Baidu academic
[Du, Yanwei]'s Articles
[Meng, Yan]'s Articles
[Zhu, Jun]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Du, Yanwei]'s Articles
[Meng, Yan]'s Articles
[Zhu, Jun]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

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