Quantitative proteomic study of myocardial mitochondria in urea transporter B knockout mice
文献类型：期刊论文
| 作者 | Du, Yanwei1; Meng, Yan1; Zhu, Jun2; Kang, Le1; Jia, Xiaolong1; Guo, Lirong1; Zhang, Ling1; Ye, Mingliang2; Hu, Lianghai3; Zhao, Xuejian1 |
| 刊名 | proteomics
 |
| 出版日期 | 2014-09-01 |
| 卷号 | 14期号:17-18页码:2072-2083 |
| 关键词 | Animal proteomics Heart Mitochondria Urea transporter |
| 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. |
| 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 |
| 关键词[WOS] | ut-b ; oxidative stress ; concentrating ability ; heart-failure ; cytochrome-c ; protein ; hsp60 ; apoptosis ; erythrocytes ; mutation |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000342912600015 |
| 公开日期 | 2015-11-17 |
| 源URL | [http://159.226.238.44/handle/321008/143194]  |
| 专题 | 大连化学物理研究所_中国科学院大连化学物理研究所 |
| 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 |
| 推荐引用方式 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. |
入库方式： OAI收割
来源：大连化学物理研究所
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