Abstract
The pathological process and mechanism of myocardial ischemia (MI) is very complicated, and remains unclear. An integrated proteomic-metabolomics analysis was applied to comprehensively understand the pathological changes and mechanism of MI. Male Sprague-Dawley rats were randomly divided into a mock surgery (MS) group and an MI group. The MI model was made by ligating the left anterior descending coronary artery, twenty-four hours after which, echocardiography was employed to assess left ventricular (LV) function variables. Blood samples and left ventricular tissues were collected for ELISA, metabolomics and proteomics analysis. The results showed that LV function, including ejection fraction (EF) and fractional shortening (FS), was significantly reduced and the level of cTnT in the serum increased after MI. iTRAQ proteomics showed that a total of 169 proteins were altered including 52 and 117 proteins with increased and decreased expression, respectively, which were mainly involved in the following activities: complement and coagulation cascades, tight junction, regulation of actin cytoskeleton, MAPK signaling pathway, endocytosis, NOD-like receptor signaling pathway, as well as phagosome coupled with vitamin digestion and absorption. Altered metabolomic profiling of this transition was mostly enriched in pathways including ABC transporters, glycerophospholipid metabolism, protein digestion and absorption and aminoacyl-tRNA biosynthesis. The integrated metabolomics and proteomics analysis indicated that myocardial injury after MI is closely related to several metabolic pathways, especially energy metabolism, amino acid metabolism, vascular smooth muscle contraction, gap junction and neuroactive ligand-receptor interaction. These findings may contribute to understanding the mechanism of MI and have implication for new therapeutic targets.
Highlights
myocardial ischemia (MI) is a serious cardiovascular disease with great morbidity and mortality
The level of cTnT was significantly higher for the MI group compared to the mock surgery (MS) group (Fig 1D)
The protein ratio distribution of the two groups appears in S2 Fig In brief, analyzing the quality control data indicated that the identification results were accurate and reliable
Summary
MI is a serious cardiovascular disease with great morbidity and mortality. The pathological process and mechanism of MI is very complicated; researchers have shown that microvascular dysfunction [1], inflammation [2] and cardiac fibrosis [3] are involved in MI, but the entire process remains unclear. Systems biology emphasizes the integration of the different components of the human body, including genes, proteins and metabolites, and investigates potential correlations between multiple molecular levels. In the past few decades, there have been remarkable achievements in the single omics study of MI [4, 5], but the exact mechanisms of MI are still unclear due to complex biochemical regulation at multiple levels. Among the omic study methodologies, proteomics and metabolomics reveal changes in proteins and metabolites respectively, and which in turn reflect the biological activities either ongoing or past [7]. We designed an integrated proteomic-metabolomics study, to comprehensively understand the pathological changes and the mechanisms of MI
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