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      Peripheral blood circular RNA hsa_circ_0124644 can be used as a diagnostic biomarker of coronary artery disease

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          Abstract

          The aim of the present study was to investigate the expression of circular RNAs (circRNAs) in the peripheral blood of coronary artery disease (CAD) patients and the potential use of circRNAs as diagnostic biomarkers of CAD. We first analysed peripheral blood circRNAs of 12 CAD patients and 12 control individuals by RNA microarray and found that 22 circRNAs were differentially expressed between these two groups: 12 were upregulated, and 10 were downregulated. Then, we selected 5 circRNAs as candidate biomarkers under stricter screening criteria and verified them in another group of subjects consisting of 30 control individuals and 30 CAD patients with different SYNTAX scores. These 5 circRNAs were all remarkably increased in the CAD group. Hsa_circ_0124644 had the largest area under the curve (AUC). We tested hsa_circ_0124644 in an independent cohort consisting of 115 control individuals and 137 CAD patients. After we included the risk factors for CAD, the AUC slightly increased from 0.769 (95% confidence interval = [0.710–0.827], P < 0.001) to 0.804 ([0.751–0.857], P < 0.001), and when combined with hsa_circ_0098964, the diagnostic value slightly increased. Taken together, our results suggest that hsa_circ_0124644 can be used as a diagnostic biomarker of CAD.

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          The SYNTAX Score: an angiographic tool grading the complexity of coronary artery disease.

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            Circulating microRNAs are new and sensitive biomarkers of myocardial infarction

            Aims Circulating microRNAs (miRNAs) may represent a novel class of biomarkers; therefore, we examined whether acute myocardial infarction (MI) modulates miRNAs plasma levels in humans and mice. Methods and results Healthy donors (n = 17) and patients (n = 33) with acute ST-segment elevation MI (STEMI) were evaluated. In one cohort (n = 25), the first plasma sample was obtained 517 ± 309 min after the onset of MI symptoms and after coronary reperfusion with percutaneous coronary intervention (PCI); miR-1, -133a, -133b, and -499-5p were ∼15- to 140-fold control, whereas miR-122 and -375 were ∼87–90% lower than control; 5 days later, miR-1, -133a, -133b, -499-5p, and -375 were back to baseline, whereas miR-122 remained lower than control through Day 30. In additional patients (n = 8; four treated with thrombolysis and four with PCI), miRNAs and troponin I (TnI) were quantified simultaneously starting 156 ± 72 min after the onset of symptoms and at different times thereafter. Peak miR-1, -133a, and -133b expression and TnI level occurred at a similar time, whereas miR-499-5p exhibited a slower time course. In mice, miRNAs plasma levels and TnI were measured 15 min after coronary ligation and at different times thereafter. The behaviour of miR-1, -133a, -133b, and -499-5p was similar to STEMI patients; further, reciprocal changes in the expression levels of these miRNAs were found in cardiac tissue 3–6 h after coronary ligation. In contrast, miR-122 and -375 exhibited minor changes and no significant modulation. In mice with acute hind-limb ischaemia, there was no increase in the plasma level of the above miRNAs. Conclusion Acute MI up-regulated miR-1, -133a, -133b, and -499-5p plasma levels, both in humans and mice, whereas miR-122 and -375 were lower than control only in STEMI patients. These miRNAs represent novel biomarkers of cardiac damage.
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              Endothelial cell apoptosis: biochemical characteristics and potential implications for atherosclerosis.

              The high turnover of endothelial cells (EC) in atherosclerosis suggests that an increase in the frequency of both cell proliferation and cell death is important in the pathogenesis of this common disorder. Further, increased apoptosis of EC, smooth muscle cells (SMC) and immune cells has been observed in atheromatous plaques. Many pro-atherogenic factors, including oxidized low-density lipoproteins, angiotensin II and oxidative stress, can induce EC apoptosis. Such damage to the endothelium may be an initiating event in atherogenesis since EC apoptosis may compromise vasoregulation, increase SMC proliferation, SMC migration and blood coagulation. In addition, EC overlying vascular lesions have been shown to increase their expression of pro-apoptotic proteins, such as Fas and Bax, while decreasing levels of anti-apoptotic factors. Therefore, understanding EC apoptotic pathways that are altered in atherosclerosis may enable a greater understanding of disease pathogenesis and foster the development of new therapies. The present discussion outlines the biochemical characteristics of EC apoptosis and the role that altered regulation of apoptosis plays in vasculopathy. Copyright 2001 Academic Press.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                03 January 2017
                2017
                : 7
                : 39918
                Affiliations
                [1 ]Department of Cardiology, People’s Hospital of Zhengzhou University, Zhengzhou University , Zhengzhou, China
                [2 ]Department of Cardiology, The First Affiliated Hospital of Zhejiang University, Zhejiang University , Hangzhou, China
                Author notes
                [*]

                These authors contributed equally to this work.

                Article
                srep39918
                10.1038/srep39918
                5206672
                28045102
                7e591774-6c0f-463a-8be7-b3a74f691410
                Copyright © 2017, The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 26 August 2016
                : 29 November 2016
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