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      MicroRNAs in heart and circulation during physical exercise

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          Highlights

          • •

            Exercise training is beneficial to cardiovascular system

          • •

            MicroRNAs are responsible for cardiac adaptions to exercise

          • •

            Exercise regulated microRNAs benefits heart

          • •

            MicroRNAs mediate protective effects of exercise in cardiovascular diseases

          • •

            Circulating microRNAs mediate beneficial effects of exercise

          Abstract

          Exercise training is beneficial to the cardiovascular system. MicroRNAs (miRNAs, miRs) are a class of conserved non-coding RNAs and play a wide-ranging role in the regulation of eukaryotic gene expression. Exercise training alters the expression levels of large amounts of miRNAs in the heart. In addition, circulating miRNAs appear to be regulated by exercise training. In this review, we will summarize recent advances in the regulation of miRNAs during physical exercise intervention in various cardiovascular diseases, including pathologic cardiac hypertrophy, myocardial fibrosis, ischemia-reperfusion injury, myocardial infarction, and heart failure. The regulatory role of circulating miRNAs after exercise training was also reviewed. In conclusion, miRNAs might be a valuable target for treatment of cardiovascular diseases and have great potential as biomarkers for assessment of physical performance.

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          Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis.

          Eva van Rooij, Lillian Sutherland, Jeffrey Thatcher … (2008)
          Acute myocardial infarction (MI) due to coronary artery occlusion is accompanied by a pathological remodeling response that includes hypertrophic cardiac growth and fibrosis, which impair cardiac contractility. Previously, we showed that cardiac hypertrophy and heart failure are accompanied by characteristic changes in the expression of a collection of specific microRNAs (miRNAs), which act as negative regulators of gene expression. Here, we show that MI in mice and humans also results in the dysregulation of specific miRNAs, which are similar to but distinct from those involved in hypertrophy and heart failure. Among the MI-regulated miRNAs are members of the miR-29 family, which are down-regulated in the region of the heart adjacent to the infarct. The miR-29 family targets a cadre of mRNAs that encode proteins involved in fibrosis, including multiple collagens, fibrillins, and elastin. Thus, down-regulation of miR-29 would be predicted to derepress the expression of these mRNAs and enhance the fibrotic response. Indeed, down-regulation of miR-29 with anti-miRs in vitro and in vivo induces the expression of collagens, whereas over-expression of miR-29 in fibroblasts reduces collagen expression. We conclude that miR-29 acts as a regulator of cardiac fibrosis and represents a potential therapeutic target for tissue fibrosis in general.
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            Braveheart, a long noncoding RNA required for cardiovascular lineage commitment.

            Carla A Klattenhoff, Johanna C. Scheuermann, Lauren Surface … (2013)
            Long noncoding RNAs (lncRNAs) are often expressed in a development-specific manner, yet little is known about their roles in lineage commitment. Here, we identified Braveheart (Bvht), a heart-associated lncRNA in mouse. Using multiple embryonic stem cell (ESC) differentiation strategies, we show that Bvht is required for progression of nascent mesoderm toward a cardiac fate. We find that Bvht is necessary for activation of a core cardiovascular gene network and functions upstream of mesoderm posterior 1 (MesP1), a master regulator of a common multipotent cardiovascular progenitor. We also show that Bvht interacts with SUZ12, a component of polycomb-repressive complex 2 (PRC2), during cardiomyocyte differentiation, suggesting that Bvht mediates epigenetic regulation of cardiac commitment. Finally, we demonstrate a role for Bvht in maintaining cardiac fate in neonatal cardiomyocytes. Together, our work provides evidence for a long noncoding RNA with critical roles in the establishment of the cardiovascular lineage during mammalian development. Copyright © 2013 Elsevier Inc. All rights reserved.
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              Pathophysiology of ischaemia-reperfusion injury.

              Donna Carden, D. Granger (2000)
              Reperfusion of ischaemic tissues is often associated with microvascular dysfunction that is manifested as impaired endothelium-dependent dilation in arterioles, enhanced fluid filtration and leukocyte plugging in capillaries, and the trafficking of leukocytes and plasma protein extravasation in postcapillary venules. Activated endothelial cells in all segments of the microcirculation produce more oxygen radicals, but less nitric oxide, in the initial period following reperfusion. The resulting imbalance between superoxide and nitric oxide in endothelial cells leads to the production and release of inflammatory mediators (e.g. platelet-activating factor, tumour necrosis factor) and enhances the biosynthesis of adhesion molecules that mediate leukocyte-endothelial cell adhesion. Some of the known risk factors for cardiovascular disease (hypercholesterolaemia, hypertension, and diabetes) appear to exaggerate many of the microvascular alterations elicited by ischaemia and reperfusion (I/R). The inflammatory mediators released as a consequence of reperfusion also appear to activate endothelial cells in remote organs that are not exposed to the initial ischaemic insult. This distant response to I/R can result in leukocyte-dependent microvascular injury that is characteristic of the multiple organ dysfunction syndrome. Adaptational responses to I/R injury have been demonstrated that allow for protection of briefly ischaemic tissues against the harmful effects of subsequent, prolonged ischaemia, a phenomenon called ischaemic preconditioning. There are two temporally and mechanistically distinct types of protection afforded by this adaptational response, i.e. acute and delayed preconditioning. The factors (e.g. protein kinase C activation) that initiate the acute and delayed preconditioning responses appear to be similar; however the protective effects of acute preconditioning are protein synthesis-independent, while the effects of delayed preconditioning require protein synthesis. The published literature in this field of investigation suggests that there are several potential targets for therapeutic intervention against I/R-induced microvascular injury. Copyright 2000 John Wiley & Sons, Ltd.
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                Author and article information

                Contributors
                Junjie Xiao
                Journal
                Journal ID (nlm-ta): J Sport Health Sci
                Journal ID (iso-abbrev): J Sport Health Sci
                Title: Journal of Sport and Health Science
                Publisher: Shanghai University of Sport
                ISSN (Print): 2095-2546
                ISSN (Electronic): 2213-2961
                Publication date PMC-release: 25 September 2018
                Publication date (Print): October 2018
                Publication date (Electronic): 25 September 2018
                Volume: 7
                Issue: 4
                Pages: 433-441
                Affiliations
                [a ]Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China
                [b ]Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, MA 02215, USA
                Author notes
                [* ]Corresponding author. junjiexiao@ 123456shu.edu.cn
                Article
                Publisher ID: S2095-2546(18)30082-6
                DOI: 10.1016/j.jshs.2018.09.008
                PMC ID: 6226555
                PubMed ID: 30450252
                SO-VID: f4b9114b-8a3b-4253-a6b9-723c74ab3bb7
                Copyright © © 2018 Published by Elsevier B.V. on behalf of Shanghai University of Sport.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 5 September 2018
                Date revision received : 12 September 2018
                Date accepted : 15 September 2018
                Categories
                Subject: Regular Paper

                Keywords: cardiovascular diseases,circulating micrornas,exercise,micrornas
                Data availability:
                Keywords: cardiovascular diseases, circulating micrornas, exercise, micrornas

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