Background: Acute myocardial infarction (AMI) is an acute disease with high mortality and seriously threatens human health. The identification of new effective biological markers for AMI is a prerequisite for treatment. Most proteomic studies have focused on atherosclerotic plaques, vascular cells, monocytes and platelets in the blood; however, the concentration of these factors in plasma is low, making it difficult to measure the complexity of plasma components. Moreover, some studies have examined the plasma protein of patients with acute coronary syndrome with histochemistry; however, the results are not consistent.Therefore, it is necessary to further investigate the differential proteins in the plasma of patients with AMI via proteomics to identify new biomarkers of AMI. Methods: In this study, immunodepletion of high-abundance plasma proteins followed by an isobaric tagging for relative and absolute quantitation (iTRAQ)-based quantitative proteomic approach was used to analyze plasma samples from 5 control individuals and 10 AMI patients. Results: Four hundred sixty-eight proteins were identified from two samples, and 33 proteins were differentially expressed in AMI patients compared to the controls. Among the 33 proteins, 12 proteins showed a ≥1.5-fold change between AMI and control samples. These proteins included fatty acid binding protein 3 (FABP3, ratio =6.36), creatine kinase-MB (CK-MB ratio =4.89), adenylate kinase1 (AK1 ratio =4.16), pro-platelet basic protein (PPBP ratio =3.29), creatine kinase (CK ratio =2.88), platelet factor 4 (PF4 ratio =2.62), peptidyl prolyl isomerase Cyclophilin A (PPIA ratio =2.05), Cofilin-1 (CFL1 ratio =1.81), coronin1A (CORO1A ratio =1.71), protein kinase M (PKM ratio =1.63), ribonuclease inhibitor (RNH1, ratio =1.67), and triose phosphate isomerase (TPI1 ratio =1.56). By contrast, there was a decrease of 19 proteins, such as adiponectin (ADIPOQ ratio =0.70), insulin-like growth factor binding protein6 (IGFBP6 ratio =0.70), Dickkopf-related protein 3 (DKK3 ratio =0.70) and complement 4B (C4B ratio =0.68). The most over-represented term was regulation of cell proliferation in the cellular component category of Gene Ontology (GO). The top 3 biological process terms were regulation of cell proliferation, response to wounding and wound healing. These proteins included immune proteins, blood coagulation proteins, lipid metabolism proteins, cytoskeleton proteins, energy metabolism proteins, gene regulation proteins, myocutaneous proteins, and myocardial remodeling proteins and were highly connected with each other, which indicates that the functional network of these processes contribute to the pathophysiology of AMI. Conclusions: In conclusion, the present quantitative proteomic study identified novel AMI biomarker candidates and might provide fundamental information for the development of an AMI biomarker.
Purpose: Leukotriene B4 (LTB4) and extracellular matrix metalloproteinase (EMM-PRIN) have been suggested as modulators of atherosclerotic plaque instability. is study sought to evaluate the potential diagnostic implication of LTB4 and EMMPRIN in patients with acute coronary syndrome (ACS).Methods: Patients (n=153) who underwent coronary angiography, including 105 patients diagnosed with ACS, were divided into four groups: stable angina pectoris (SAP, n=19), unstable angina pectoris (UAP, n=39), acute myocardial infarction (AMI, n=66) and control (with normal coronary angiography, n=29). EMMPRIN expression in peripheral blood mononuclear cells was determined by ow cytometry and serum LTB4 levels were measured by ELISA. To examine whether LTB4 can regulate the expression of EMM-PRIN and matrix metalloproteinases (MMPs) in macrophages, di erentiated THP-1 macrophages were stimulated with di erent concentrations of LTB4 (10-10-10-7mmol/ L). Expression of EMMPRIN was evaluated by Western blotting. MMP-9 mRNA expression and enzymatic activity were determined by RT-PCR and SDS-PAGE gelatin zymography.Result: Serum LTB4 concentration was signi cantly higher in AMI and UAP groups, compared with control and SAP groups (p<0.01). Subgroups analysis showed that LTB4 was signi cantly higher in the AMI<24h group, compared with the AMI>24h group. Expression of EMMPRIN on circulating monocytes was signi cantly higher in patients with UAP and AMI (>24h), compared with control, SAP and AMI (<24h) groups (p<0.05). In vitro study showed LTB4 up-regulated the expression of EMMPRIN, as well as the expression and activity of MMP-9, in cultured THP-1-derived macrophages (p<0.05).Conclusion: LTB4 and EMMPRIN are associated with the pathogenesis of ACS and may be potential biomarkers for patients with ACS.
A 55-year-old man who suffered from acute myocardial infarction complicated with cardiogenic shock was administered veno-arterial extracorporeal membrane oxygenation. Ultra-high pre-membrane lung oxygen saturation of 93% was observed. Transthoracic echocardiography revealed the presence of patent foramen ovale. The four-chamber view showed that the tip of the cannula was located in the patent foramen ovale, which resulted in a left-to-right shunt. Without adjusting the position of the drainage cannula, the patient was weaned from extracorporeal membrane oxygenation at 136 hours after initiation and survived to hospital discharge.
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