Serum Of Myocardial Infarction Patients Research Articles

Synthesis , Characterization and Study the Effect of Benzothiazol-pyrazole Derivatives on the Activity of AST, ALT Enzymes

This work includes synthesis some of 2-(4,5-dihydro-1H-pyrazol-1-yl)-1,3-benzothiazole derivatives which synthesized from 2-hydrazino-1,3-benzothiazole with dicarbonyl compounds. The prepared compounds were characterized by FT-IR, 1HNMR and also studied the physical properties. The effect of the biological activity for these compounds were studied on the activity of AST and ALT enzymes in human serum of myocardial infarction patients. The studies show the compounds (A2 and A5) caused inhibition while the compound (A3 and A4) caused activation for the activity for AST and ALT enzymes.

LncRNA KCNQ1OT1 as a miR-26a-5p sponge regulates ATG12-mediated cardiomyocyte autophagy and aggravates myocardial infarction

BackgroundAs a dominant cardiovascular disease, myocardial infarction (MI) causes a considerable mortality globally. KCNQ1 overlapping transcript 1 (KCNQ1OT1) was reported to be overexpressed in MI patients. However, the detailed mechanisms remain unclear. MethodsWe analyzed the expression of KCNQ1OT1 in the serum of MI patients, and built ischemia/reperfusion (I/R) mouse and H/R-induced cell model. TTC staining was used to evaluate infarct size in mice. TUNEL was employed to assess cell apoptosis. QRT-PCR was performed to detect the expression of KCNQ1OT1 and miR-26a-5p. The formation of autophagosomes in cells was detected by immunofluorescence. Caspase3 activity was detected by the Caspase-3 Assay Kit. Autophagy and apoptosis-related proteins were assessed by western blotting. Luciferase reporter assay was used to assess the binding relationship of KCNQ1OT1 and miR-26a-5p and miR-20a-5p/ATG12. ResultsKCNQ1OT1 was up-regulated while miR-26a-5p was decreased in MI patients, I/R mouse and H/R-induced cell model. KCNQ1OT1 knockdown inhibited cell autophagy and protected cardiomyocytes from apoptosis by up-regulating miR-26a-5p. Either KCNQ1OT1 knockdown or miR-26a-5p mimics caused inhibition of autophagy related 12 homolog (ATG12), which was the direct target of miR-26a-5p. In vivo, KCNQ1OT1 promoted cardiomyocytes apoptosis via miR-26a-5p/ATG12 pathway. ConclusionKCNQ1OT1/miR-26a-5p/ATG12 axis regulated cardiomyocyte autophagy and apoptosis, both in vivo and in vitro. These data supported that KCNQ1OT1 inhibition might be a promising therapeutic option for protection after MI.

Exosome Derived from Coronary Serum of Patients with Myocardial Infarction Promotes Angiogenesis Through the miRNA-143/IGF-IR Pathway.

PurposeMyocardial ischemia-reperfusion injury primarily causes myocardial infarction (MI), which is manifested by cell death. Angiogenesis is essential for repair and regeneration in cardiac tissue after MI. In this study, we aimed to investigate the effect of exosomes derived from the serum of MI patients in angiogenesis and its related mechanism.Patients and MethodsExosomes, isolated from serum, were collected from MI (MI-exosome) and control (Con-exosome) patients. After coculturing with human umbilical vein endothelial cells, MI-exosome promoted cell proliferation, migration, and tube formation.ResultsThe results revealed that the production and release of MI-exosome were associated with cardiomyocytes. Moreover, microarray assays demonstrated that miRNA-143 was significantly decreased in MI-exosome. Meanwhile, the overexpression and knockdown of miRNA-143 could inhibit and enhance angiogenesis, respectively. Furthermore, the effect of exosomal miRNA-143 on angiogenesis was mediated by its targeting gene, insulin-like growth factor 1 receptor (IGF-IR), and was associated with the production of nitric oxide (NO).ConclusionTaken together, exosomes derived from the serum of patients with MI promoted angiogenesis through the IGF-IR/NO signaling pathway. The results provide novel understanding of the function of exosomes in MI.

Profiling thiol metabolites in myocardial infarction human serum by stable isotope labeling assisted liquid chromatography-mass spectrometry

Myocardial Infarction (MI) is one of the most common causes of deaths worldwide. Thiols have been reported to play a key role in physiological and pathological processes of MI. Comprehensive analysis of thiols would be conducive to fully elucidate the relation between thiols and MI. In the current study, we analyze the metabolomic differences of thiols in serum between MI patients (n = 30) and healthy controls (HCs, n = 30) by stable isotope labeling-dispersive solid phase extraction-liquid chromatography-full scan-Orbitrap-mass spectrometry analysis (IL-DSPE-LC-full scan-Orbitrap MS) method. We detected 300 potential thiols in serum of MI patients and HCs, among which, 67 thiols were positively or putatively identified. Furthermore, we found that the levels of 71 thiols in serum exhibited significant difference between MI patients and HCs. In the transsulfuration pathway, we observed that Cys and Hcys were upregulated, while GSH were downregulated. Our results provide a comprehensive understanding of thiols metabolome in human serum between MI patients and HCs.

Serum of patients with acute myocardial infarction prevents inflammation in iPSC-cardiomyocytes

Acute myocardial infarction (MI) evokes a systemic inflammatory response and locally the degradation of the necrotic tissue, followed by scar formation. The mechanisms for containment of the infarct zone are not studied well. The study aimed to examine the response of healthy cardiomyocytes to serum of patients with myocardial infarction. Human iPSC-cardiomyocytes (iPSC-CM) generated from two healthy donors were incubated with serum of patients with MI with and without ventricular fibrillation (VF) or of healthy controls. Different cell adhesion molecules were studied by flow cytometry and immunostaining. Cellular electrophysiology was studied by patch clamp. The cell adhesion molecules CD54/ICAM-1, CD58/LFA-3 and CD321/JAM-A were expressed on iPSC-CM within the plasma membrane. Incubation with serum of MI patients reduced the levels of expression of CD54/ICAM-1 and CD321/JAM-A by 15–20%. VF serum was less effective than serum of MI patients without VF. MI serum or VF serum did not affect resting potential, action potential duration or maximum depolarization velocity. Myocardial infarction serum exerts anti-inflammatory effects on healthy cardiomyocytes without affecting their electrical activity, thus helping to contain the infarct zone and to protect healthy tissue. Ventricular fibrillation during MI drives healthy cardiomyocytes towards a pro-inflammatory phenotype.

Association of MIR-499a expression and seed region variant (rs3746444) with cardiovascular disease in Egyptian patients

Background: Circulating microRNAs could be powerful markers of acute myocardial infarction (MI) and its functional genetic variants could increase susceptibility to cardiovascular disease (CVD). The current study aimed to quantify the microRNA (miR)-499a levels in serum of MI patients compared to hypertensive and healthy subjects and to investigate the association of its A/G variant rs3746444 with CVD in a sample of an Egyptian population.Methods: Serum miR-499a relative expressions were measured in 110 acute MI patients, 76 hypertensive patients, and 121 healthy controls by Real-time quantitative polymerase chain reaction. MIR-499a genotyping was performed for an additional 107 coronary artery disease patients by Real-time allele discrimination assay.Results: Acute MI patients showed high relative expression of miR-499a (> 105-fold, p < .001), and it was nearly undetectable in healthy controls and hypertensive patients. It showed an area under the curve of 0.953, with a sensitivity of 97.2% and a specificity of 75.0%. ST-elevation MI (STEMI) patients had higher miR-499a serum levels than patients with Non-STEMI. There was a significant association of MIR-499a variant with acute MI but not with hypertension under all genetic models tested. As a new finding, in overall and stratified analysis, the miR-499a variant was not correlated with its expression profile.Conclusions: Circulating miR-499a levels could be a useful biomarker, discriminating acute MI within 12 hours from healthy subjects. Its variant rs3746444 A/G is associated with increased susceptibility to acute MI and CAD in Egyptian population.

Abundant and Altered Expression of PIWI-Interacting RNAs during Cardiac Hypertrophy.

The discovery of PIWI-interacting RNAs (piRNAs) has fundamentally changed our understanding of post transcriptional regulation of transposons and other genes. Unlike miRNA and siRNA, the piRNAs are the most abundant but least studied RNA species in mammals. Although the expression of PIWI proteins and piRNAs has long been regarded as germline specific, increasing evidences suggest the expression of piRNAs in somatic cells. In this study, the small RNA sequencing executed during induction of cardiac hypertrophy in both in vivo and in vitro conditions were annotated for the expression of piRNAs. The expression of piRNAs was validated by qPCR and RNA immunoprecipitation. In addition, the presence of piRNAs in circulation of myocardial infarction patients was studied by qPCR. We identified an abundant and altered expression of piRNAs during cardiac hypertrophy. The differentially expressed piRNAs was validated by qPCR and RNA immunoprecipitation. The significantly and differentially expressed piRNAs were predicted to target different retrotransposons and mRNAs in the rat genome. The detection of specific piRNA in serum of myocardial infarction patients suggests the potential of piRNA for diagnosis. Overall this study is the first to provide a whole-genome analysis of the large repertoire of piRNAs in the cardiac system and this would pave a new path to understanding the molecular aetiology of piRNA and retrotransposons in the physiology and pathology of the cardiac system.

Hematological and Biochemical Variations in Myocardial Infarction

Background: The aim of the current study was to assess the hematological and biochemical variations in the serum of myocardial infarction patients and healthy controls. Method: The case-control study included 200 samples collected from Myocardial infarction patients and controls for the analysis the variations of hematological and biochemical. Result: WBC and ESR were increased, whereas, hemoglobin and platelet was decreased in patients as compared with the controls. Serum triglyceride, total cholesterol, LDL increased and decreased HDL in patients as compared with the controls. Copper and potassium showed increased levels whereas, decreased serum albumin, and zinc in patients as compared with the controls. Conclusion: Further detailed investigations on the role of hematological, biochemical, variations in the pathogenesis of acute myocardial infarction are needed.

Study of Some Physiological and Biochemical Aspects in The Serum of Myocardial Infarction Patients

Study of Some Physiological and Biochemical Aspects in The Serum of Myocardial Infarction Patients

Cytochrome-c detection: a diagnostic marker for myocardial infarction.

Following a myocardial infarction (MI) cells die or are damaged and their contents leak into the blood circulation, resulting in elevated serum levels of various enzymes, proteins, and organic molecules. Over the past few decades, it has become standard practice to employ the detection of these elevated substances as markers for the confirmation of MIs and to monitor MI patients' response to treatment. Although it has previously been shown that cytochrome-c, a small respiratory protein, is among those elevated, the lack of a suitable detection system has prevented its routine use in the diagnosis of MIs. We present a preliminary study in which chemiluminescence was employed to detect elevated levels of cytochrome-c in the serum of MI patients. The technique, which is specific for c-type proteins, is approx 30 times more sensitive than the traditional Coomassie blue stain and can detect as little as 0.03 microg of protein. It also has potential for diagnostic use in other diseases that are characterized by mitochondrial damage.