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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.
Crippa, Stefania; Nemir, Mohamed; Ounzain, Samir; Ibberson, Mark; Berthonneche, Corinne; Sarre, Alexandre; Boisset, Gaëlle; Maison, Damien; Harshman, Keith; Xenarios, Ioannis; Diviani, Dario; Schorderet, Daniel; Pedrazzini, Thierry.
Afiliación
  • Crippa S; Experimental Cardiology Unit, Department of Medicine, University of Lausanne Medical School, Lausanne 1011, Switzerland.
  • Nemir M; Experimental Cardiology Unit, Department of Medicine, University of Lausanne Medical School, Lausanne 1011, Switzerland.
  • Ounzain S; Experimental Cardiology Unit, Department of Medicine, University of Lausanne Medical School, Lausanne 1011, Switzerland.
  • Ibberson M; Swiss Institute of Bioinformatics, Lausanne, Switzerland.
  • Berthonneche C; Cardiovascular Assessment Facility, University of Lausanne, Lausanne, Switzerland.
  • Sarre A; Cardiovascular Assessment Facility, University of Lausanne, Lausanne, Switzerland.
  • Boisset G; Institute for Research in Ophthalmology, Sion, Switzerland.
  • Maison D; Experimental Cardiology Unit, Department of Medicine, University of Lausanne Medical School, Lausanne 1011, Switzerland.
  • Harshman K; Lausanne Genomic Technologies Facility, University of Lausanne, Lausanne, Switzerland.
  • Xenarios I; Swiss Institute of Bioinformatics, Lausanne, Switzerland.
  • Diviani D; Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.
  • Schorderet D; Institute for Research in Ophthalmology, Sion, Switzerland.
  • Pedrazzini T; Experimental Cardiology Unit, Department of Medicine, University of Lausanne Medical School, Lausanne 1011, Switzerland thierry.pedrazzini@chuv.ch.
Cardiovasc Res ; 110(1): 73-84, 2016 May 01.
Article en En | MEDLINE | ID: mdl-26857418
AIMS: The adult mammalian heart has poor regenerative capacity. In contrast, the zebrafish heart retains a robust capacity for regeneration into adulthood. These distinct responses are consequences of a differential utilization of evolutionary-conserved gene regulatory networks in the damaged heart. To systematically identify miRNA-dependent networks controlling cardiac repair following injury, we performed comparative gene and miRNA profiling of the cardiac transcriptome in adult mice and zebrafish. METHODS AND RESULTS: Using an integrated approach, we show that 45 miRNA-dependent networks, involved in critical biological pathways, are differentially modulated in the injured zebrafish vs. mouse hearts. We study, more particularly, the miR-26a-dependent response. Therefore, miR-26a is down-regulated in the fish heart after injury, whereas its expression remains constant in the mouse heart. Targets of miR-26a involve activators of the cell cycle and Ezh2, a component of the polycomb repressive complex 2 (PRC2). Importantly, PRC2 exerts repressive functions on negative regulators of the cell cycle. In cultured neonatal cardiomyocytes, inhibition of miR-26a stimulates, therefore, cardiomyocyte proliferation. Accordingly, miR-26a knockdown prolongs the proliferative window of cardiomyocytes in the post-natal mouse heart. CONCLUSIONS: This novel strategy identifies a series of miRNAs and associated pathways, in particular miR-26a, which represent attractive therapeutic targets for inducing repair in the injured heart.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Cicatrización de Heridas / MicroARNs / Proliferación Celular / Redes Reguladoras de Genes Límite: Animals Idioma: En Revista: Cardiovasc Res Año: 2016 Tipo del documento: Article País de afiliación: Suiza Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Cicatrización de Heridas / MicroARNs / Proliferación Celular / Redes Reguladoras de Genes Límite: Animals Idioma: En Revista: Cardiovasc Res Año: 2016 Tipo del documento: Article País de afiliación: Suiza Pais de publicación: Reino Unido