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      Effect of microRNA-133a-3p/matrix metalloproteinase-9 axis on the growth of atherosclerotic vascular smooth muscle cells

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          Abstract

          Atherosclerosis (AS) is the leading cause of cardiovascular disease and poses a threat to human health. MicroRNAs (miRNAs/miRs) are a group of endogenous small non-coding RNAs that have been identified to serve important roles in AS. However, the expression and role of miR-133a-3p in AS remains unclear. The aim of the present study was to investigate miR-133a-3p in AS and to determine its underlying mechanism. The level of miR-133a-3p expression in the blood and vascular plaque tissue of patients with AS was detected via reverse transcription-quantitative PCR (RT-qPCR). The role of miR-133a-3p in human vascular smooth muscle cells (hVSMCs) was investigated, following upregulation and downregulation of this miR in hVSMCs. Cell proliferation and apoptosis were determined using a Cell Counting kit-8 assay and flow cytometry, respectively. The results demonstrated the downregulation of miR-133a-3p in the blood and vascular plaque tissue of patients with AS. Matrix metallopeptidase-9 (MMP-9) was revealed to be a direct target gene of miR-133a-3p, which was upregulated in the blood and vascular plaque tissue of patients with AS. Furthermore, MMP-9 was determined to be negatively regulated by miR-133a-3p in hVSMCs. In addition, significant inhibition of hVSMC proliferation and induction of cell apoptosis were observed following MMP-9 downregulation and following transfection with the miR-133a-3p mimic. The effects of the miR-133a-3p mimic on hVSMC proliferation and apoptosis were reversed by MMP-9 over-expression. Overall, the results indicated that miR-133a-3p was downregulated in AS, which results in the inhibition of hVSMC proliferation and the induction of cell apoptosis via MMP-9. miR-133a-3p may therefore be a promising therapeutic target for the treatment of AS.

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          Most cited references 24

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          Roles for microRNAs in conferring robustness to biological processes.

          Biological systems use a variety of mechanisms to maintain their functions in the face of environmental and genetic perturbations. Increasing evidence suggests that, among their roles as posttranscriptional repressors of gene expression, microRNAs (miRNAs) help to confer robustness to biological processes by reinforcing transcriptional programs and attenuating aberrant transcripts, and they may in some network contexts help suppress random fluctuations in transcript copy number. These activities have important consequences for normal development and physiology, disease, and evolution. Here, we will discuss examples and principles of miRNAs that contribute to robustness in animal systems. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Biogenesis, turnover, and mode of action of plant microRNAs.

            MicroRNAs (miRNAs) are small RNAs that control gene expression through silencing of target mRNAs. Mature miRNAs are processed from primary miRNA transcripts by the endonuclease activity of the DICER-LIKE1 (DCL1) protein complex. Mechanisms exist that allow the DCL1 complex to precisely excise the miRNA from its precursor. Our understanding of miRNA biogenesis, particularly its intersection with transcription and other aspects of RNA metabolism such as splicing, is still evolving. Mature miRNAs are incorporated into an ARGONAUTE (AGO) effector complex competent for target gene silencing but are also subjected to turnover through a degradation mechanism that is beginning to be understood. The mechanisms of miRNA target silencing in plants are no longer limited to AGO-catalyzed slicing, and the contribution of translational inhibition is increasingly appreciated. Here, we review the mechanisms underlying the biogenesis, turnover, and activities of plant miRNAs.
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              MicroRNA Regulation of Atherosclerosis.

              Atherosclerosis and its attendant clinical complications, such as myocardial infarction, stroke, and peripheral artery disease, are the leading cause of morbidity and mortality in Western societies. In response to biochemical and biomechanical stimuli, atherosclerotic lesion formation occurs from the participation of a range of cell types, inflammatory mediators, and shear stress. Over the past decade, microRNAs (miRNAs) have emerged as evolutionarily conserved, noncoding small RNAs that serve as important regulators and fine-tuners of a range of pathophysiological cellular effects and molecular signaling pathways involved in atherosclerosis. Accumulating studies reveal the importance of miRNAs in regulating key signaling and lipid homeostasis pathways that alter the balance of atherosclerotic plaque progression and regression. In this review, we highlight current paradigms of miRNA-mediated effects in atherosclerosis progression and regression. We provide an update on the potential use of miRNAs diagnostically for detecting increasing severity of coronary disease and clinical events. Finally, we provide a perspective on therapeutic opportunities and challenges for miRNA delivery in the field.
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                Author and article information

                Journal
                Exp Ther Med
                Exp Ther Med
                ETM
                Experimental and Therapeutic Medicine
                D.A. Spandidos
                1792-0981
                1792-1015
                December 2019
                01 October 2019
                01 October 2019
                : 18
                : 6
                : 4356-4362
                Affiliations
                [1 ]Department of Emergency Internal Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266071, P.R. China
                [2 ]Department of Interventional Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266071, P.R. China
                [3 ]Department of Cardiovascular Medicine, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, P.R. China
                Author notes
                Correspondence to: Dr Shanglang Cai, Department of Cardiovascular Medicine, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao, Shandong 266000, P.R. China, E-mail: caisl201717@ 123456163.com
                Article
                ETM-0-0-8070
                10.3892/etm.2019.8070
                6861869
                8694986e-f162-4e8b-a4bb-8daedd1af0f6
                Copyright: © Shi et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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