Journal
ONCOTARGET
Volume 8, Issue 29, Pages 48321-48332Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.15689
Keywords
dilated cardiomyopathy; left ventricle; cell death; S100A1; eEF2
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Funding
- National Key Basic Research Program of China [2014CBA02003, 2013CB910802]
- MOST 863 program [2014AA020902]
- Natural Science Foundation of Shanghai [16ZR1402400, 15DZ2291100]
- Zhuo Xue Program of Fudan University
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Dilated cardiomyopathy (DCM) is caused by reduced left ventricular (LV) myocardial function, which is one of the most common causes of heart failure (HF). We performed iTRAQ-coupled 2D-LC-MS/MS to profile the cardiac proteome of LV tissues from healthy controls and patients with end-stage DCM. We identified 4263 proteins, of which 125 were differentially expressed in DCM tissues compared to LV controls. The majority of these were membrane proteins related to cellular junctions and neuronal metabolism. In addition, these proteins were involved in membrane organization, mitochondrial organization, translation, protein transport, and cell death process. Four key proteins involved in the cell death process were also detected by western blotting, indicated that cell death was activated in DCM tissues. Furthermore, S100A1 and eEF2 were enriched in the cellular assembly and organization and cell cycle networks, respectively. We verified decreases in these two proteins in end-stage DCM LV samples through multiple reaction monitoring (MRM). These observations demonstrate that our understanding of the mechanisms underlying DCM can be deepened through comparison of the proteomes of normal LV tissues with that from end-stage DCM in humans.
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