MicroRNAs Play an Essential Role in the Development of Cardiac Hypertrophy

Sayed, Danish; Hong, Chull; Chen, Ieng-Yi; Lypowy, Jacqueline; Abdellatif, Maha

doi:10.1161/01.res.0000257913.42552.23

Cited by 709 publications

(625 citation statements)

References 35 publications

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“…Abdellatif's group found that miR-1 was singularly downregulated as early as day 1, persisting through day 7, after TAC-induced hypertrophy in a mouse model (6). Overexpression of miR-1 carried by adenovirus vector inhibited its in silico-predicted growth-related targets, including Ras guanosine-triphosphatase-activating protein, cyclin-dependent kinase 9, fibronectin, and Ras homolog enriched in brain, in addition to protein synthesis and cell size (Fig.…”

Section: Micrornas and Cardiac Hypertrophy And Heart Failurementioning

confidence: 95%

“…Recently, since 2005, the exciting research on the biological roles of miRNAs in the mammalian cardiovascular system has become a most rapidly evolving field. Several studies have demonstrated the importance of miRNAs not only in cardiovascular development, but also in cardiovascular disease (5)(6)(7)(8). In the present article, the currently relevant findings on the role of miRNAs in cardiac hypertrophy and heart failure will be summarized and the target genes and signaling pathways linking these miRNAs in the context will be discussed.…”

Section: Introductionmentioning

confidence: 94%

“…The two models of pathological cardiac hypertrophy demonstrated that the expression of miRNAs are both up-and downregulated during differently induced cardiac hypertrophy. Sayed et al reported an array of more than 50 microRNAs with expression that progressively changes during development of pressure-overload cardiac hypertrophy and identified miR-1 as among the earliest microRNAs downregulated during hypertrophy (6).…”

Section: Expression Profiles Of Mirnas In the Cardiac Hypertrophy Andmentioning

confidence: 99%

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Role of microRNAs in cardiac hypertrophy and heart failure

et al. 2009

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SummaryMicroRNAs (miRNAs) are a class of endogenous, highly conserved, small noncoding RNAs that regulate gene expression post-transcriptionally. Recent studies have demonstrated that miRNAs are aberrantly expressed in the cardiovascular system. The implications of miRNAs in cardiovascular disease have recently been recognized, representing the most rapidly evolving research field. Gain-and loss-of-function studies in mice models have identified distinct roles for specific miRNAs during cardiac hypertrophy, heart failing, and myocardial infarction. In the present article, the currently relevant findings on the role of miRNAs in cardiac hypertrophy and heart failure will be summarized and the target genes and signaling pathways linking these miRNAs will be discussed. Furthermore, we focus on the use of miRNA mimics and antagonists (antagomirs) as tools for disease therapy in the cardiovascular system in the future. Taken together, the recent studies showed that miRNAs are key regulators of gene expression in cardiovascular biology and suggested the potential importance of miRNAs as diagnostic markers and therapeutic targets for cardiovascular disease.2009 IUBMB IUBMB Life, 61(6): 566-571, 2009

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Section: Micrornas and Cardiac Hypertrophy And Heart Failurementioning

confidence: 95%

Section: Introductionmentioning

confidence: 94%

Section: Expression Profiles Of Mirnas In the Cardiac Hypertrophy Andmentioning

confidence: 99%

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Role of microRNAs in cardiac hypertrophy and heart failure

et al. 2009

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“…For example, the work on miRNAs has been focused especially on hypertrophy, heart failure, and the control of electrical activity in the heart. Several studies have reported that some miRNAs are either increased (e.g., miR-195) [27] or decreased (e.g., miR-1, miR-133) [28] in response to dysregulated ion dynamics during pathological heart conditions. Importantly, alterations in the expression of miRNA may underlie the process producing the dysfunctional cardiac excitability and arrhythmic death [29].…”

Section: Mirnas and Alterations Of Their Expression In Response To MImentioning

confidence: 99%

Ion channels/transporters as epigenetic regulators? —a microRNA perspective

Jiang

Zhang

Chan

2012

Sci. China Life Sci.

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MicroRNA (miRNA) alterations in response to changes in an extracellular microenvironment have been observed and considered as one of the major mechanisms for epigenetic modifications of the cell. While enormous efforts have been made in the understanding of the role of miRNAs in regulating cellular responses to the microenvironment, the mechanistic insight into how extracellular signals can be transduced into miRNA alterations in cells is still lacking. Interestingly, recent studies have shown that ion channels/transporters, which are known to conduct or transport ions across the cell membrane, also exhibit changes in levels of expression and activities in response to changes of extracellular microenvironment. More importantly, alterations in expression and function of ion channels/transporters have been shown to result in changes in miRNAs that are known to change in response to alteration of the microenvironment. In this review, we aim to summarize the recent data demonstrating the ability of ion channels/transporters to transduce extracellular signals into miRNA changes and propose a potential link between cells and their microenvironment through ion channels/transporters. At the same time, we hope to provide new insights into epigenetic regulatory mechanisms underlying a number of physiological and pathological processes, including embryo development and cancer metastasis. ion channel, miRNAs, epigenetic, microenvironment

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“…More and more evidences have been shown that miRNAs have critical roles in participating and regulating various cardiovascular diseases, such as cardiac arrhythmia 4, cardiac hypertrophy 5, 6, cardiac injuries 7 and finally the heart failure 8. It has been reported that several miRNAs are involved in the development and progression of cardiac fibrosis.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐503 promotes angiotensin II‐induced cardiac fibrosis by targeting Apelin‐13

Zhou

Lin

Zhao

et al. 2016

J Cellular Molecular Medi

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Cardiac fibrosis is a major cause of heart failure. MicroRNAs (miRs) are important epigenetic regulators of cardiac function and cardiovascular diseases, including cardiac fibrosis. This study aimed to explore the role of miR‐503 and its mechanisms in regulating cardiac fibrosis. miR‐503 was found up‐regulated in the mouse LV tissues subjected to transverse aortic constriction (TAC) and in neonatal cardiac fibroblasts (CFs) cultured with Angiotension II. The role of miR‐503 in regulating CF cell proliferation and/or collagen production in mice neonatal CFs were determined using an MTT assay and RT‐PCR respectively. Forced expression of miR‐503 increased the cellular proliferation and collagen production in mice neonatal CFs. The effects were abrogated by cotransfection with AMO‐503 (a specific inhibitor of miR‐503). Injection of antagomiR‐503 elevated cardiac function and inhibited the expression of connective tissue growth factor (CTGF) and transforming growth factor (TGF)‐β in the TAC mice. Additional analysis revealed that Apelin‐13 is a direct target of miR‐503, as the overexpression of miR‐503 decreased the protein and mRNA expression levels of Apelin‐13. In the CFs with pre‐treatment of AngII, we transfected AMO‐503 into the cells treated with siRNA‐APLN. siRNA‐APLN abolished the effects of AMO‐503 on the production of collagen I and III and the expression of TGF‐β and CTGF. Furthermore, pre‐treatment of CFs with Apelin‐13 (1–100 nmol/l) inhibited angiotensin II‐mediated collagen production and activation of CTGF and TGF‐β. So we conclude that miR‐503 promotes cardiac fibrosis via miR‐503‐Apelin‐13‐TGF‐β‐CTGF‐collagen production pathway. Thus, miR‐503 is a promising therapeutic target for reducing cardiac fibrosis.

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MicroRNAs Play an Essential Role in the Development of Cardiac Hypertrophy

Cited by 709 publications

References 35 publications

Role of microRNAs in cardiac hypertrophy and heart failure

Role of microRNAs in cardiac hypertrophy and heart failure

Ion channels/transporters as epigenetic regulators? —a microRNA perspective

MicroRNA‐503 promotes angiotensin II‐induced cardiac fibrosis by targeting Apelin‐13

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