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      Knockdown of circROBO2 attenuates acute myocardial infarction through regulating the miR-1184/TRADD axis

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          Abstract

          Background

          Studies have found that circular RNAs (circRNAs) play key roles in cardiovascular diseases. However, the function of circROBO2 in acute myocardial infarction (AMI) is unclear. This study aimed to investigate the pathogenesis of circROBO2 in AMI.

          Methods

          qRT-PCR and Western blot were used to determine the expression levels of circROBO2, miR-1184, and TRADD in AMI and sham-operated mouse models at mRNA and protein level, respectively. The relationship among miR-1184, circROBO2 and TRADD was evaluated by RNA immunoprecipitation (RIP) analysis and luciferase reporter gene analysis. The roles of circROBO2, miR-1184, and TRADD in myocardial cell apoptosis were evaluated using flow cytometry. Ultrasound echocardiography, serum creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH), myocardial infarction area, and myocardial cell apoptosis were measured to examine the effects of circROBO2 on myocardial injury.

          Results

          The expression levels of miR-1184 were significantly reduced, and the expression levels of circROBO2 and TRADD were significantly increased in MI group. CircROBO2 acted as a sponge for miR-1184 by upregulating the expression of TRADD. In addition, overexpression of miR-1184 enhanced the protective effect of knockdown of circROBO2 by partially inhibiting the expression of TRADD in vivo and in vitro.

          Conclusion

          Knockdown of circROBO2 reduced the apoptosis of cardiomyocytes by increasing the expression levels of miR-1184, which in turn decreased the expression levels of TRADD in the myocardium post-MI.

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          Acute Myocardial Infarction.

          Jeffrey Anderson, David A Morrow (2017)
          Article 0 comments Cited 280 times – based on 0 reviews     Review now
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            The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge.

            Bernard Gersh, Gerd Heusch (2017)
            The incidence of ST segment elevation myocardial infarction (STEMI) has decreased over the last two decades in developed countries, but mortality from STEMI despite widespread access to reperfusion therapy is still substantial as is the development of heart failure, particularly among an expanding older population. In developing countries, the incidence of STEMI is increasing and interventional reperfusion is often not available. We here review the pathophysiology of acute myocardial infarction and reperfusion, notably the temporal and spatial evolution of ischaemic and reperfusion injury, the different modes of cell death, and the resulting coronary microvascular dysfunction. We then go on to briefly characterize the cardioprotective phenomena of ischaemic preconditioning, ischaemic postconditioning, and remote ischaemic conditioning and their underlying signal transduction pathways. We discuss in detail the attempts to translate conditioning strategies and drug therapy into the clinical setting. Most attempts have failed so far to reduce infarct size and improve clinical outcomes in STEMI patients, and we discuss potential reasons for such failure. Currently, it appears that remote ischaemic conditioning and a few drugs (atrial natriuretic peptide, exenatide, metoprolol, and esmolol) reduce infarct size, but studies with clinical outcome as primary endpoint are still underway.
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              PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock

              Holger Thiele, Ibrahim Akin, Marcus Sandri … (2017)
              In patients who have acute myocardial infarction with cardiogenic shock, early revascularization of the culprit artery by means of percutaneous coronary intervention (PCI) improves outcomes. However, the majority of patients with cardiogenic shock have multivessel disease, and whether PCI should be performed immediately for stenoses in nonculprit arteries is controversial.
              Article 0 comments Cited 192 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Tian-ping Chen:
                ORCID: http://orcid.org/0000-0002-0188-1263
                ra3330@163.com
                Journal
                Journal ID (nlm-ta): Mol Med
                Journal ID (iso-abbrev): Mol Med
                Title: Molecular Medicine
                Publisher: BioMed Central (London )
                ISSN (Print): 1076-1551
                ISSN (Electronic): 1528-3658
                Publication date (Electronic): 3 March 2021
                Publication date PMC-release: 3 March 2021
                Publication date Collection: 2021
                Volume: 27
                Electronic Location Identifier: 21
                Affiliations
                GRID grid.414884.5, Department of Cardiology, , the First Affiliated Hospital of Bengbu Medical College, ; No. 287, Changhuai Road, Longzi Lake District, Bengbu city, 233003 Anhui province China
                Author information
                http://orcid.org/0000-0002-0188-1263
                Article
                Publisher ID: 275
                DOI: 10.1186/s10020-021-00275-6
                PMC ID: 7931513
                PubMed ID: 33658002
                SO-VID: 4d6e471f-e79a-494e-a5bc-87d96dcc74ce
                Copyright © © The Author(s) 2021
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 1 April 2020
                Date accepted : 20 January 2021
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                Keywords: circrobo2,mir-1184,tradd,acute myocardial infarction,apoptosis
                Data availability:
                Keywords: circrobo2, mir-1184, tradd, acute myocardial infarction, apoptosis

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