Any medium, provided the original work is properly credited. The
PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/22026160 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Laborde et al. Proteome Science 2014, 12:43 http://www.proteomesci.com/content/12/1/Page 2 ofCurrent clinical criteria for the diagnosis of ACS established by the European Society of Cardiology (ESC) and the American Heart Association (AHA) include the determination of plasma levels of troponin and the heart type creatine kinase
PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13485127 isoenzyme (CKMB) [11]. However, in both cases, their plasma levels are not elevated until 4? hours after onset of symptoms, which undoubtedly leads a delay in diagnosis. In this sense, it is necessary the identification of new biomarkers transferable to clinical practice. Its introduction would help to establish an early diagnosis of the disease, could provide new therapeutic targets on which to develop drugs, or could permit monitoring the evolution of patients on a specific treatment and thus to establish a correct prognosis. In the present study, the objective was to discover whether there was a common protein profile between patients who have suffered a non-ST segment elevation acute coronary syndrome (NSTEACS) and patients who have suffered a ST segment elevation acute coronary syndrome (STEACS) or whether the greater hypoxia at which the myocardium is subjected in the second case and consequently the greater extent of tissue necrosis produced the existence of a characteristic proteomic profile.Why could be hypoxia important in ACS proteome?Biochemical disorders that occur in ischemic heart disease are consequence of hypoxia. Under restricted oxygen conditions, the muscular cells of the myocardium obtain energy from anaerobic glycolysis, resulting in lactate accumulation. This excess of lactate causes an intracellular acidosis that leads to the activation of proteolytic enzymes, to degradation of structural proteins responsible for cardiac contractility, to the loss of integrity of the cell membrane and, ultimately, to the release of proteins to the blood and to the intercellular gap due to cell death. In this process, the proteins that first appear in the circulation are cytoplasmic (myoglobin and cytoplasmic creatine kinase), followed by mitochondrial proteins (mitochondrial creatine kinase) and structural proteins (troponins and myosin). This explains why different plasma levels of these current
Ethyl (4,5,6,7-tetrahydrothiazolo[5,4-c]pyridin-2-yl)carbamate hydrochloride clinical
3-(tert-Butyldimethylsilyloxy)propan-1-amine biomarkers permit the clinicians to theoretically classify the extension of an ACS.(p < 0.05, 13 upregulated and 11 downregulated, Table 2), respectively. These differentially expressed spots were excised from silver stained gels, digested with trypsin and analyzed by MALDI-TOF/TOF. The ensuing database search identified 23 differentially expressed proteins in NSTEACS patients vs healthy controls and 11 in STEACS patients vs healthy controls. The spot maps of both analyses are shown in Figure 1 and complete data of identified spots are shown in Tables 1 and 2. Principal component analysis (PCA) was used to reduce the complexity of the multidimensional dataset, providing a clearer overview to better reveal trends within the data. In both 2D-DIGE analyses, this analysis efficiently discriminated NSTEACS (Figure 2A) or STEACS patients (Figure 2B) from healthy controls plasma samples with perfect separation of samples by the first principal component (PC1). In this plot,.