Plasma proteomics implicate glutamic oxaloacetic transaminases as potential markers for acute myocardial infarction

Abstract

AimTo provide a novel perspective on the pathogenesis of acute myocardial infarction (AMI) patients with respect to glutamic oxaloacetic transaminase (GOT). MethodsThe plasma proteome of 20 patients with AMI were matched for age and sex and compared with 10 healthy individuals. We analyzed the mass spectrum data and compared the signal intensity of the corresponding peptides which related to their corresponding proteins. A sample-specific protein database was constructed and a quality control analysis was conducted to screen out the key regulatory proteins under specific experimental conditions. The data from 37 new AMI patients and 13 healthy adults were subjected to parallel reaction monitoring (PRM) to verify the target proteins found. Finally, the survival status of the key genes (> 1.5-fold) in the PPI were analyzed. Results2589 and 2162 proteins were identified and quantified, respectively, and 143 differentially expressed proteins (DEPs) (≥1.5-fold) were found between the AMI and control groups. Of these 90 and 53 were significantly up-regulated and down-regulated, respectively. Gene ontology, KEGG enrichment, protein domain and cluster analysis as well as PPI networks of the DEPs revealed a central role of acute inflammatory response processes in patients with AMI. A cluster of proteins were found to be related to cysteine, methionine, arginine, proline, phenylalanine and propanoate metabolism as well as the cAMP signaling pathway. PPI network analysis showed CHI3L1, COPB2, GOT2, MB, CYCS, GOT1, CKM, SAA1 and PRKCD and RPS3 were in key positions, but only MB, CKM, GOT1, PRKCD, CYCS and GOT2 were found in a cluster. PRM verified the high levels of MB, CKM, GOT1 and GOT2 in 37 AMI patients but there was no statistical difference in the survival status for patients with either high or low expression levels of these proteins. ConclusionsOur findings showed that acute inflammatory response processes play a central role in patients with AMI. Cysteine and methionine metabolism was also activated, in which GOT1 and GOT2 were key proteins. These pathways might be potential targets for diagnosis and novel therapies to improve the poor outcomes observed in patients with heart failure.