دورية أكاديمية
Therapeutic Delivery of miR-148a Suppresses Ventricular Dilation in Heart Failure.
| العنوان: | Therapeutic Delivery of miR-148a Suppresses Ventricular Dilation in Heart Failure. |
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| المؤلفون: | Raso A; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., Dirkx E; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy., Philippen LE; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX, USA., Fernandez-Celis A; Cardiovascular Translational Research, Navarrabiomed, Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona, Spain., De Majo F; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., Sampaio-Pinto V; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; Instituto de Investigação e Inovação em Saúde (i3S), Porto, Portugal; Instituto Nacional de Engenharia Biomédica (INEB), Porto, Portugal; Instituto de Ciências Biomédicas de Abel Salazar (ICBAS), Universidade do Porto, Porto, Portugal., Sansonetti M; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., Juni R; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., El Azzouzi H; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; Departments of Cardiology and Pathology, University Medical Center Utrecht, Utrecht, the Netherlands., Calore M; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., Bitsch N; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., Olieslagers S; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands., Oerlemans MIFJ; Departments of Cardiology and Pathology, University Medical Center Utrecht, Utrecht, the Netherlands., Huibers MM; Departments of Cardiology and Pathology, University Medical Center Utrecht, Utrecht, the Netherlands., de Weger RA; Departments of Cardiology and Pathology, University Medical Center Utrecht, Utrecht, the Netherlands., Reckman YJ; Department of Experimental Cardiology, Amsterdam UMC location AMC, Amsterdam, the Netherlands., Pinto YM; Department of Experimental Cardiology, Amsterdam UMC location AMC, Amsterdam, the Netherlands., Zentilin L; International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy., Zacchigna S; International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy; Department of Medicine, Surgery and Health Sciences, University of Trieste, Italy., Giacca M; International Centre for Genetic Engineering and Biotechnology (ICGEB), Trieste, Italy; Department of Medicine, Surgery and Health Sciences, University of Trieste, Italy., da Costa Martins PA; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal., López-Andrés N; Cardiovascular Translational Research, Navarrabiomed, Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona, Spain., De Windt LJ; Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands. Electronic address: l.dewindt@maastrichtuniversity.nl. |
| المصدر: | Molecular therapy : the journal of the American Society of Gene Therapy [Mol Ther] 2019 Mar 06; Vol. 27 (3), pp. 584-599. Date of Electronic Publication: 2018 Nov 17. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Cell Press Country of Publication: United States NLM ID: 100890581 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1525-0024 (Electronic) Linking ISSN: 15250016 NLM ISO Abbreviation: Mol Ther Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2017- : Cambridge, MA : Cell Press Original Publication: San Diego, CA : Academic Press, 2000- |
| مواضيع طبية MeSH: | Cardiomyopathies/*metabolism , Heart Failure/*metabolism , Heart Transplantation/*methods , MicroRNAs/*metabolism , Myocardium/*metabolism, Animals ; Cardiomyopathies/genetics ; Cell Proliferation/physiology ; Heart Failure/genetics ; Humans ; Mice ; MicroRNAs/genetics ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Signal Transduction/physiology ; Ventricular Remodeling/genetics ; Ventricular Remodeling/physiology |
| مستخلص: | Heart failure is preceded by ventricular remodeling, changes in left ventricular mass, and myocardial volume after alterations in loading conditions. Concentric hypertrophy arises after pressure overload, involves wall thickening, and forms a substrate for diastolic dysfunction. Eccentric hypertrophy develops in volume overload conditions and leads wall thinning, chamber dilation, and reduced ejection fraction. The molecular events underlying these distinct forms of cardiac remodeling are poorly understood. Here, we demonstrate that miR-148a expression changes dynamically in distinct subtypes of heart failure: while it is elevated in concentric hypertrophy, it decreased in dilated cardiomyopathy. In line, antagomir-mediated silencing of miR-148a caused wall thinning, chamber dilation, increased left ventricle volume, and reduced ejection fraction. Additionally, adeno-associated viral delivery of miR-148a protected the mouse heart from pressure-overload-induced systolic dysfunction by preventing the transition of concentric hypertrophic remodeling toward dilation. Mechanistically, miR-148a targets the cytokine co-receptor glycoprotein 130 (gp130) and connects cardiomyocyte responsiveness to extracellular cytokines by modulating the Stat3 signaling. These findings show the ability of miR-148a to prevent the transition of pressure-overload induced concentric hypertrophic remodeling toward eccentric hypertrophy and dilated cardiomyopathy and provide evidence for the existence of separate molecular programs inducing distinct forms of myocardial remodeling. (Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.) |
| التعليقات: | Comment in: Mol Ther. 2019 Mar 6;27(3):489-490. (PMID: 30777607) |
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| فهرسة مساهمة: | Keywords: adeno-associated vector; cardiac; heart failure; hypertrophy; miR-148a; microRNA; signaling |
| المشرفين على المادة: | 0 (MicroRNAs) 0 (Mirn148 microRNA, mouse) 0 (STAT3 Transcription Factor) |
| تواريخ الأحداث: | Date Created: 20181219 Date Completed: 20191216 Latest Revision: 20200309 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC6403487 |
| DOI: | 10.1016/j.ymthe.2018.11.011 |
| PMID: | 30559069 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1525-0024 |
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| DOI: | 10.1016/j.ymthe.2018.11.011 |