Journal
JOURNAL OF PROTEOMICS
Volume 197, Issue -, Pages 14-22Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jprot.2019.01.021
Keywords
Sudden cardiac death; Lethal ventricular tachyarrhythmia; Lipidomics; Proteomics; Mitochondrial dysfunction
Categories
Funding
- Natural Science Foundation [2015A408119346049]
- Science and Technology Innovation project of Guangdong Province [2013KJCX0076]
- Natural Science Foundation of Shanghai [15ZR1430300]
- Shanghai Sailing Program, China [16YF140800]
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Lethal ventricular tachyarrhythmia (LVTA) is the most prevalent electrophysiological event leading to sudden cardiac death (SCD). In this study, the myocardial lipidome and proteome were analysed in rats experiencing LVTA as a consequence of acute myocardial ischemia (AMI). Results showed that 257 lipid species and 814 myocardial proteins were disrupted during LVTA_ Cardiolipin (CL), phosphatidylcholine (PC), phosphatidylethanolamine (PE), ceramide (Car), lysophosphatidylethanolamine (LPE), lysophosphatidylcholine (LPC), phosphatidylglycerol (PG), and lysophosphatidylserine (LPS) were down-regulated; whereas sphingosine (SO) and diacylglycerol (DG) were up-regulated. Enrichment analysis of these proteins suggested mitochondriai dysfunction. Most of the differential lipids showed a high degree of interaction with the core differentially expressed proteins. Seven lipid pathways, including DG -> PE, PE -> LPE, PA -> DG, PC -> DG, PE -> PA, Cer -> SM, and LPE -> LPC, were active during the process. Activation of LPE -> PE could be partially confirmed by proteomic results. CL (72:7), PE (42:4), and LPE (P-18:0) jointly represent a promising diagnostic markers for LVTA. Collectively, we discovered marked disturbances of the lipidome and proteome in the myocardia of LVTA rats, mainly involving dysfunction of the mitochondrial respiratory chain.
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