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      Plasma MIR-212-3p as a biomarker for acute right heart failure with pulmonary artery hypertension

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          Abstract

          Background

          Acute right heart failure occurs in patients with pulmonary artery hypertension (PAH) with exposure to acute inflammation, the mortality rate is very high when right heart failure occurs. Biomarkers that can be used to detect acute right heart failure in patients with pulmonary hypertension need to be studied.

          Methods

          A PAH rat model was established using monocrotaline, and lipopolysaccharide was used to induce acute right heart failure. The Agilent rat miRNA microarray, Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to assess the microRNA expression of PAH rats. The expression of up- and downregulated miRNAs in plasma from PAH patients with acute right heart failure was validated with quantitative reverse transcription polymerase chain reaction (qRT-PCR). Then, the Wilcoxon matched paired test and receiver operating characteristic (ROC) curve analysis were performed.

          Results

          Thirty-three miRNAs were upregulated, and 7 miRNAs were downregulated in plasma of PAH rats with acute right heart failure. In the plasma of PAH patients, the miR-212-3p level was inversely correlated with the level of NT-pro BNP, and the area under the ROC curve was 0.751.

          Conclusions

          These results suggest that the reduction of the expression of MIR-212-3p may be a biomarker for PAH patients with right heart dysfunction.

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          Most cited references37

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          The functions of animal microRNAs.

          Victor Ambros (2004)
          MicroRNAs (miRNAs) are small RNAs that regulate the expression of complementary messenger RNAs. Hundreds of miRNA genes have been found in diverse animals, and many of these are phylogenetically conserved. With miRNA roles identified in developmental timing, cell death, cell proliferation, haematopoiesis and patterning of the nervous system, evidence is mounting that animal miRNAs are more numerous, and their regulatory impact more pervasive, than was previously suspected.
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            Activation of a HIF1alpha-PPARgamma axis underlies the integration of glycolytic and lipid anabolic pathways in pathologic cardiac hypertrophy.

            Jaya Krishnan, Marianne Suter, Renata Windak … (2009)
            Development of cardiac hypertrophy and progression to heart failure entails profound changes in myocardial metabolism, characterized by a switch from fatty acid utilization to glycolysis and lipid accumulation. We report that hypoxia-inducible factor (HIF)1alpha and PPARgamma, key mediators of glycolysis and lipid anabolism, respectively, are jointly upregulated in hypertrophic cardiomyopathy and cooperate to mediate key changes in cardiac metabolism. In response to pathologic stress, HIF1alpha activates glycolytic genes and PPARgamma, whose product, in turn, activates fatty acid uptake and glycerolipid biosynthesis genes. These changes result in increased glycolytic flux and glucose-to-lipid conversion via the glycerol-3-phosphate pathway, apoptosis, and contractile dysfunction. Ventricular deletion of Hif1alpha in mice prevents hypertrophy-induced PPARgamma activation, the consequent metabolic reprogramming, and contractile dysfunction. We propose a model in which activation of the HIF1alpha-PPARgamma axis by pathologic stress underlies key changes in cell metabolism that are characteristic of and contribute to common forms of heart disease.
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              Hypoxia-inducible factor-1 is central to cardioprotection: a new paradigm for ischemic preconditioning.

              Tobias Eckle, Rainer Lehmann, Karim El Khatib … (2008)
              Ischemic preconditioning provides strong cardioprotection from ischemia, but its molecular mechanisms remain unknown. Convincing evidence confirms a central role of hypoxia-inducible factor (HIF)-1 in mammalian oxygen homeostasis. Thus, we pursued HIF-1 as a central component of cardioprotection by ischemic preconditioning. Murine studies of in situ preconditioning revealed a robust activation of cardiac HIF-1. Moreover, in vivo small interfering RNA repression of cardiac HIF-1 resulted in abolished cardioprotection by ischemic preconditioning. In contrast, pretreatment with the HIF activator dimethyloxalylglycine was associated with cardioprotection similar to that of ischemic preconditioning itself. Finally, selective small interfering RNA repression of prolylhydroxylase 2 resulted in significant activation of HIF-1 alpha and attenuated myocardial infarct sizes (0.44+/-0.09-fold). As an end point of HIF-dependent cardioprotection, we defined the role of A2B adenosine receptor (A2BAR) signaling. Although the cardiac A2BAR was induced with HIF activation, HIF-dependent cardioprotection was abolished in A2BAR-/- mice. Taken together, these studies provide evidence for a critical role of HIF-1 in ischemic preconditioning via enhancing purinergic signaling pathways.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Transl Med
                Journal ID (iso-abbrev): Ann Transl Med
                Journal ID (publisher-id): ATM
                Title: Annals of Translational Medicine
                Publisher: AME Publishing Company
                ISSN (Print): 2305-5839
                ISSN (Electronic): 2305-5847
                Publication date (Print and electronic): December 2020
                Publication date (Print): December 2020
                Volume: 8
                Issue: 23
                Electronic Location Identifier: 1571
                Affiliations
                [1 ]Department of Anesthesiology, Xiangya Hospital Central South University , Changsha, China;
                [2 ]National Clinical Research Center for Geriatric Disorders, Xiangya Hospital Central South University , Changsha, China;
                [3 ]Key Laboratory of Biological Nanotechnology of National Health Commission , Changsha, China
                Author notes

                Contributions: (I) Conception and design: E Wang, Y Yang; (II) Administrative support: E Wang, Q Guo; (III) Provision of study materials or patients: E Wang, S Luo, S Dai; (IV) Collection and assembly of data: R Li, S Dai; (V) Data analysis and interpretation: Y Cao; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

                Correspondence to: E. Wang. Department of Anesthesiology, Xiangya Hospital Central South University, Changsha, China. Email: ewang324@ 123456csu.edu.cn .
                [^]

                ORCID: 0000-0001-9463-9769.

                Article
                Publisher ID: atm-08-23-1571
                DOI: 10.21037/atm-20-1653a
                PMC ID: 7791226
                PubMed ID: 33437770
                SO-VID: a76da692-040d-4bb3-ad4a-c8555b171140
                Copyright © 2020 Annals of Translational Medicine. All rights reserved.
                License:

                Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

                History
                Date received : 19 February 2020
                Date accepted : 10 October 2020
                Categories
                Subject: Original Article

                Keywords: microrna,right heart failure,pulmonary hypertension,inflammation
                Data availability:
                Keywords: microrna, right heart failure, pulmonary hypertension, inflammation

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