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      miRNA 206 and miRNA 574-5p are highly expression in coronary artery disease

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          Abstract

          Our studies demonstrate two miRNAs ( miR-206 and miR-574-5p) that are significantly up-regulated in coronary artery disease (CAD) patients as compared with healthy controls, and the two miRNAs can be potential non-invasive biomarkers for early detection of CAD.

          Abstract

          Coronary artery disease (CAD) is the leading cause of human morbidity and mortality worldwide. Innovative diagnostic biomarkers are a pressing need for this disease. miRNAs profiling is an innovative method of identifying biomarkers for many diseases and could be proven as a powerful tool in the diagnosis and treatment of CAD. We performed miRNA microarray analysis from the plasma of three CAD patients and three healthy controls. Subsequently, we performed quantitative real-time PCR (qRT-PCR) analysis of miRNA expression in plasma of another 67 CAD patients and 67 healthy controls. We identified two miRNAs ( miR-206 and miR-574-5p) that were significantly up-regulated in CAD patients as compared with healthy controls ( P<0.05). The receiver operating characteristic (ROC) curves indicated these two miRNAs had great potential to provide sensitive and specific diagnostic value for CAD.

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          Most cited references23

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          Serum response factor regulates a muscle-specific microRNA that targets Hand2 during cardiogenesis.

          Gradients of signalling and transcription factors govern many aspects of embryogenesis, highlighting the need for spatiotemporal control of regulatory protein levels. MicroRNAs are phylogenetically conserved small RNAs that regulate the translation of target messenger RNAs, providing a mechanism for protein dose regulation. Here we show that microRNA-1-1 (miR-1-1) and miR-1-2 are specifically expressed in cardiac and skeletal muscle precursor cells. We found that the miR-1 genes are direct transcriptional targets of muscle differentiation regulators including serum response factor, MyoD and Mef2. Correspondingly, excess miR-1 in the developing heart leads to a decreased pool of proliferating ventricular cardiomyocytes. Using a new algorithm for microRNA target identification that incorporates features of RNA structure and target accessibility, we show that Hand2, a transcription factor that promotes ventricular cardiomyocyte expansion, is a target of miR-1. This work suggests that miR-1 genes titrate the effects of critical cardiac regulatory proteins to control the balance between differentiation and proliferation during cardiogenesis.
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            Pathophysiology of coronary artery disease.

            During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.
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              The Drosophila microRNA Mir-14 suppresses cell death and is required for normal fat metabolism.

              MicroRNAs (miRNAs) are small regulatory RNAs that are between 21 and 25 nucleotides in length and repress gene function through interactions with target mRNAs. The genomes of metazoans encode on the order of several hundred miRNAs, but the processes they regulate have been defined for only two in C. elegans. We searched for new inhibitors of apoptotic cell death by testing existing collections of P element insertion lines for their ability to enhance a small-eye phenotype associated with eye-specific expression of the Drosophila cell death activator Reaper. Here we report the identification of the Drosophila miRNA mir-14 as a cell death suppressor. Loss of mir-14 enhances Reaper-dependent cell death, whereas ectopic expression suppresses cell death induced by multiple stimuli. Animals lacking mir-14 are viable. However, they are stress sensitive and have a reduced lifespan. Mir-14 mutants have elevated levels of the apoptotic effector caspase Drice, suggesting one potential site of action. Mir-14 also regulates fat metabolism. Deletion of mir-14 results in animals with increased levels of triacylglycerol and diacylglycerol, whereas increases in mir-14 copy number have the converse effect. We discuss possible relationships between these phenotypes.
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                Author and article information

                Journal
                Biosci Rep
                Biosci. Rep
                ppbioscirep
                BSR
                Bioscience Reports
                Portland Press Ltd.
                0144-8463
                1573-4935
                18 December 2015
                10 February 2016
                February 2016
                : 36
                : 1 ( displayID: 1 )
                : e00295
                Affiliations
                [* ]Ningbo Medical Center, Lihuili Hospital, Ningbo University, Ningbo, Zhejiang 315041, P.R. China
                []Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, Zhejiang 315211, P.R. China
                []Diabetes Research Center, School of Medicine, Ningbo University, Ningbo, Zhejiang 315211, P.R. China
                [§ ]Department of Pathology, Key Laboratory of Antibody Technique of Ministry of Health, Nanjing Medical University, Nanjing 210029, P.R. China
                Author notes
                [1]

                These authors are co-first authors of this work.

                [ 2 ]Correspondence may be addressed to either of these authors (email liuns@ 123456njmu.edu.cn or hjmpin@ 123456163.com ).
                Article
                e00295
                10.1042/BSR20150206
                4748332
                26685009
                5b63306b-eb60-4a6d-b36d-b9451a9edd5f
                © 2016 Authors

                This is an open access article published by Portland Press Limited and distributed under the Creative Commons Attribution Licence 3.0.

                History
                : 11 August 2015
                : 26 November 2015
                : 1 December 2015
                Page count
                Figures: 4, Tables: 1, References: 34, Pages: 7
                Categories
                Original Papers
                Original Paper

                Life sciences
                biomarker,coronary artery disease,mirna,plasma
                Life sciences
                biomarker, coronary artery disease, mirna, plasma

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