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      Circulating MicroRNAs: Biogenesis and Clinical Significance in Acute Myocardial Infarction

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          Abstract

          Acute myocardial infarction (AMI) causes many deaths around the world. Early diagnosis can prevent the development of AMI and provide theoretical support for the subsequent treatment. miRNAs participate in the AMI pathological processes. We aim to determine the early diagnostic and the prognostic roles of circulating miRNAs in AMI in the existing studies and summarize all the data to provide a greater understanding of their utility for clinical application. We reviewed current knowledge focused on the AMI development and circulating miRNA formation. Meanwhile, we collected and analyzed the potential roles of circulating miRNAs in AMI diagnosis, prognosis and therapeutic strategies. Additionally, we elaborated on the challenges and clinical perspectives of the application of circulating miRNAs in AMI diagnosis. Circulating miRNAs are stable in the circulation and have earlier increases of circulating levels than diagnostic golden criteria. In addition, they are tissue and disease-specific. All these characteristics indicate that circulating miRNAs are promising biomarkers for the early diagnosis of AMI. Although there are several limitations to be resolved before clinical use, the application of circulating miRNAs shows great potential in the early diagnosis and the prognosis of AMI.

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          miR-145 and miR-143 Regulate Smooth Muscle Cell Fate Decisions

          Kimberly Cordes, Neil T. Sheehy, Mark White … (2009)
          SUMMARY microRNAs are regulators of myriad cellular events, but evidence for a single microRNA that can efficiently differentiate multipotent cells into a specific lineage or regulate direct reprogramming of cells into an alternate cell fate has been elusive. Here, we show that miR-145 and miR-143 are co-transcribed in multipotent cardiac progenitors before becoming localized to smooth muscle cells, including neural crest stem cell–derived vascular smooth muscle cells. miR-145 and miR-143 were direct transcriptional targets of serum response factor, myocardin and Nkx2.5, and were downregulated in injured or atherosclerotic vessels containing proliferating, less differentiated smooth muscle cells. miR-145 was necessary for myocardin-induced reprogramming of adult fibroblasts into smooth muscle cells and sufficient to induce differentiation of multipotent neural crest stem cells into vascular smooth muscle. Furthermore, miR-145 and miR-143 cooperatively targeted a network of transcription factors, including Klf4, myocardin, and Elk-1 to promote differentiation and repress proliferation of smooth muscle cells. These findings demonstrate that miR-145 can direct the smooth muscle fate and that miR-145 and miR-143 function to regulate the quiescent versus proliferative phenotype of smooth muscle cells.
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            MiR-33 contributes to the regulation of cholesterol homeostasis.

            Katey Rayner, Yajaira Suárez, Alberto Davalos … (2010)
            Cholesterol metabolism is tightly regulated at the cellular level. Here we show that miR-33, an intronic microRNA (miRNA) located within the gene encoding sterol-regulatory element-binding factor-2 (SREBF-2), a transcriptional regulator of cholesterol synthesis, modulates the expression of genes involved in cellular cholesterol transport. In mouse and human cells, miR-33 inhibits the expression of the adenosine triphosphate-binding cassette (ABC) transporter, ABCA1, thereby attenuating cholesterol efflux to apolipoprotein A1. In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-density lipoprotein (HDL). Lentiviral delivery of miR-33 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels. Conversely, silencing of miR-33 in vivo increases hepatic expression of ABCA1 and plasma HDL levels. Thus, miR-33 appears to regulate both HDL biogenesis in the liver and cellular cholesterol efflux.
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              MicroRNA-92a controls angiogenesis and functional recovery of ischemic tissues in mice.

              Angelika Bonauer, Guillaume Carmona, Masayoshi Iwasaki … (2009)
              MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression by binding to target messenger RNAs (mRNAs), leading to translational repression or degradation. Here, we show that the miR-17approximately92 cluster is highly expressed in human endothelial cells and that miR-92a, a component of this cluster, controls the growth of new blood vessels (angiogenesis). Forced overexpression of miR-92a in endothelial cells blocked angiogenesis in vitro and in vivo. In mouse models of limb ischemia and myocardial infarction, systemic administration of an antagomir designed to inhibit miR-92a led to enhanced blood vessel growth and functional recovery of damaged tissue. MiR-92a appears to target mRNAs corresponding to several proangiogenic proteins, including the integrin subunit alpha5. Thus, miR-92a may serve as a valuable therapeutic target in the setting of ischemic disease.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Physiol
                Journal ID (iso-abbrev): Front Physiol
                Journal ID (publisher-id): Front. Physiol.
                Title: Frontiers in Physiology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-042X
                Publication date (Electronic): 03 September 2020
                Publication date Collection: 2020
                Volume: 11
                Electronic Location Identifier: 1088
                Affiliations
                [1] 1Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao University , Qingdao, China
                [2] 2The Affiliated Hospital of Qingdao University, Qingdao University , Qingdao, China
                Author notes

                Edited by: Joaquin Garcia-Estañ, University of Murcia, Spain

                Reviewed by: Antonio Longo, University of Catania, Italy; Gang Yuan, Huazhong University of Science and Technology, China

                *Correspondence: Lei Zhang, leizhang@ 123456qdu.edu.cn

                This article was submitted to Integrative Physiology, a section of the journal Frontiers in Physiology

                Article
                DOI: 10.3389/fphys.2020.01088
                PMC ID: 7494963
                PubMed ID: 33013463
                SO-VID: 341b463d-ecaf-4edc-ab94-a0a6559c2e6d
                Copyright © Copyright © 2020 Zhang, Ding, Zhang, Wang, Zhu and Li.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 01 April 2020
                Date accepted : 06 August 2020
                Page count
                Figures: 2, Tables: 2, Equations: 0, References: 141, Pages: 16, Words: 0
                Funding
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Categories
                Subject: Physiology
                Subject: Review

                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: acute myocardial infarction,diagnosis,circulating micrornas,biomarkers,challenges
                Data availability:
                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: acute myocardial infarction, diagnosis, circulating micrornas, biomarkers, challenges

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