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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways

ABSTRACT: The mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. 2 conditions, 6 biological replicates per condition

ORGANISM(S): Mus musculus

SUBMITTER: Mark Ibberson

PROVIDER: E-GEOD-51012 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.

Crippa Stefania S Nemir Mohamed M Ounzain Samir S Ibberson Mark M Berthonneche Corinne C Sarre Alexandre A Boisset Gaëlle G Maison Damien D Harshman Keith K Xenarios Ioannis I Diviani Dario D Schorderet Daniel D Pedrazzini Thierry T

Cardiovascular research 20160207 1

<h4>Aims</h4>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 an ...[more]

PMID: 26857418

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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways

Project description:The mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. 2 conditions, 4 biological replicates per condition

2016-02-18 | E-GEOD-51013 | biostudies-arrayexpress

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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways

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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways

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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways

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Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Long RNA Seq on Sham vs MI Adult Mouse Heart

Project description:We systematically identified, annotated and characterised the mouse long non-coding transcriptome during myocardial infarction, revealing hundreds of novel heart specific lncRNAs with unique functional and regulatory characteristics. 2 conditions, 4 biological replicates per condition

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H3K27me3 deposition over sarcomeric and cytoskeletal promoters is required for cardiomyocyte cytokinesis and wound invasion during zebrafish heart regeneration [ChIP-seq]

Project description:Deciphering the genetic and epigenetic regulation of injury-induced heart regeneration in organisms capable of robust cardiac renewal represents an attractive inroad towards regenerating the human heart. In the highly regenerative zebrafish heart, cardiomyocytes near the wound edge undergo dramatic gene expression changes concomitant with sarcomere disassembly, loss of cell-cell adhesion, and detachment from the extracellular matrix (ECM), which leaves them poised to divide and give rise to new muscle cells that colonize the wound. Using integrated high-throughput transcriptional and chromatin analyses, we identified correlations between gene expression changes and activating H3K4me3 and/or repressive H3K27me3 dynamics in cardiomyocytes following injury. Within the category of downregulated genes that gain H3K27me3, transcripts encoding sarcomere and cytoskeletal components were significantly overrepresented. To investigate a functional requirement for H3K27me3-mediated gene silencing during zebrafish heart regeneration, we generated an inducible transgenic strain expressing a mutant version of histone 3, H3.3K27M, which allowed us to inhibit H3K27me3 catalysis in cardiomyocytes during the regenerative window. Hearts composed of H3.3K27M-expressing cardiomyocytes fail to regenerate with wound edge myocardium showing heightened expression of structural genes and prominent sarcomere structures. Although cell cycle re-entry was unperturbed, cytokinesis and wound invasion were significantly compromised. Collectively, our study identifies a requirement for H3K27me3-mediated silencing of structural genes during zebrafish heart regeneration and suggests that repression of similar structural components in the border zone of the infarcted human heart might improve its regenerative capacity.

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