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Proteomics. 2014 Sep;14(17-18):2072-83. doi: 10.1002/pmic.201400123. Epub 2014 Aug 8.

Quantitative proteomic study of myocardial mitochondria in urea transporter B knockout mice.

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  • 1Key Laboratory of Pathobiology, Department of Pathophysiology, Ministry of Education, College of Basic Medicine, Jilin University, Changchun, P. R. China.


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 O2 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 (ΔΨm) 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.

© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Animal proteomics; Heart; Mitochondria; Urea transporter

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