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

PROVIDER: PRJNA219631 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR997328.fastq.gz	Fastqsanger.gz
	SRR997329.fastq.gz	Fastqsanger.gz
	SRR997330.fastq.gz	Fastqsanger.gz
	SRR997331.fastq.gz	Fastqsanger.gz
	SRR997332.fastq.gz	Fastqsanger.gz

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Macrophages directly contribute collagen to scar formation during zebrafish heart regeneration and mouse heart repair

Project description:The adult mammalian heart heals after myocardial infarction (MI) by deposition of scar tissue, leading to downstream arrhythmia, remodelling and heart failure1. In contrast, adult zebrafish and neonatal mouse hearts are capable of regenerating after injury. Macrophages are key mediators of tissue repair and appear to be required for both regeneration and healing by scar formation, but the mechanisms underlying these distinct roles are poorly understood2-4. Here we investigated how macrophages differentially influence the mode of repair by determining their responses in scar-free versus scar-induced healing, comparing ventricular resection with cryo-injured adult zebrafish hearts and neonatal versus adult mouse hearts after MI. Unbiased transcriptomics revealed molecular programmes implicating macrophages in the initiation and resolution of inflammation to dictate the kinetics of scarring during zebrafish regeneration and the activation of direct and indirect pathways to drive fibrosis in the adult mouse heart. Most notably we observed up-regulation of collagen isoforms in both zebrafish and mouse macrophages following injury. Adoptive transfer of macrophages, from resected zebrafish hearts into cryo-injured hosts and splenic monocyte-derived macrophages from adult mouse donors into neonatal hearts, enhanced scar formation and induced fibrosis, respectively, via cell autonomous production of collagen. In zebrafish, macrophage-specific targeting of collagen 4a binding protein and cognate collagen 4a1 followed by transfer led to significantly reduced scarring in cryo-injured hosts, as further evidence of a direct macrophage contribution to collagen deposition and scar formation. These findings contrast with the current model of scarring, whereby collagen is laid down exclusively by myofibroblasts, and implicate macrophages as critical regulators of heart repair.

2019-12-18 | GSE126772 | GEO

Inhibition of TGF-β/Smad3 signaling disrupts cardiomyocyte cell cycle progression and EMT-like migration during ventricle regeneration

Project description:Transcriptome sequencing of SIS3-treated uninjured (5dpf) and injured (2dpt) zebrafish hearts.

2021-04-07 | GSE162820 | GEO

Genomeâ??wide transcriptional profiling with spatial resolution identifies Bone Morphogenetic Protein signaling as essential regulator of zebrafish cardiomyocyte regeneration.

Project description:In contrast to mammals, zebrafish regenerate heart injuries via proliferation of cardiomyocytes located at the wound border. Here, we show that tomo-seq can be used to identify whole-genome transcriptional profiles of the injury zone, the border zone and the healthy myocardium. Interestingly, the border zone is characterized by the re-expression of embryonic cardiac genes that are also activated after myocardial infarction in mouse and human, including targets of Bone Morphogenetic Protein (BMP) signaling. Endogenous BMP signaling has been reported to be detrimental to mammalian cardiac repair. In contrast, we find that genetic or chemical inhibition of BMP signaling in zebrafish reduces cardiomyocyte dedifferentiation and proliferation, ultimately compromising myocardial regeneration, while bmp2b overexpression is sufficient to enhance it. Our results provide a resource for further studies on the molecular regulation of cardiac regeneration and reveal intriguing differential cellular responses of cardiomyocytes to a conserved signaling pathway in regenerative versus non-regenerative hearts. To generate spatially-resolved RNA-seq data for injured zebrafish hearts (3 and 7 days-post-injury), we cryosectioned samples, extracted RNA from the individual sections, and amplified and barcoded mRNA using the CEL-seq protocol (Hashimshony et al., Cell Reports, 2012) with a few modifications. Libraries were sequenced on Illumina NextSeq using 75bp paired end sequencing.

2016-01-11 | E-GEOD-74652 | biostudies-arrayexpress

Comparison of the gene expression expression profile of activated and resting epicardium

Project description:Zebrafish can regenerate their hearts. As a first response to injury, the epicardium reacts by upregulalion of developmental marker genes. Here we compared in an unbiased manner the expression of the epicardium from uninjured zebrafish hearts and hearts at 3 days postcryoinjury. To label epicardial cells of uninjured hearts we usd pard3:GFP (POon et al 2010) and to label epicardium of the injured heart wt1b:eGFP (Perner et al 2007)

2019-07-30 | GSE118457 | GEO

Gene expression arrays of cardiomyocyte ribosome-associated RNAs during zebrafish heart regeneration

Project description:A transgenic line cmlc2:TRAP was made to express EGFP-fused ribosomal protein L10a (EGFP-L10a) in zebrafish cardiomyocytes. Then ribosome-associated RNAs were immuoprecipitated from uninjured and injured adult cmlc2:TRAP fish to determine the differential expression changes during zebrafish heart regeneration. A nine chip study with cardiomyocyte ribosome associated RNAs purified from three separate isolation of uninjured adult cmlc2:TRAP fish hearts, three separate isolation of 1 day post amupation (dpa) adult cmlc2:TRAP fish hearts, and three separate isolation of 7 dpa adult cmlc2:TRAP fish hearts.

2013-08-01 | E-GEOD-48914 | biostudies-arrayexpress

Transcription profiling of injured mouse hearts from C57Bl/6 and MRL sampled at 3 time points to investigate the regenerative capacity of the mammalian heart

Project description:Previous studies have suggested that the heart may be capable of limited repair and regeneration in response to a focal injury while other studies indicate that the mammalian heart has no regenerative capacity. To further explore this issue, we performed a series of superficial and transmural myocardial injuries in C57BL/6 and MRL/MpJ adult mice. At defined time intervals following the respective injury (Days 3, 14, 30 and 60) we examined cardiac function using echocardiography, morphology, FACS cell sorting for BrdU positive cells and molecular signature using microarray analysis. We observed complete restoration of myocardial function in the superficial MRL cryoinjured heart and significantly less scar formation as compared to the injured hearts of C57BL/6 mice. Following a severe transmural myocardial injury, the MRL mouse has increased survival and decreased ventricular remodeling compared to the C57BL/6 mouse but without evidence of significant regeneration. The cytoprotective program observed in the severely injured MRL heart is in part due to increased vasculogenesis and decreased apoptosis that limits the extension of the injury. We conclude that C57BL/6 and MRL injured hearts have evidence of limited myocardial regeneration, in response to superficial injury, but the improved function and survival observed in the MRL mouse heart following severe injury is not due to significant regenerative processes. Mouse hearts from C57BL/6 and MRL/MpJ strains were injured with LAD ligation and harvested at 3, 30 and 60 days after treatement.

2007-11-23 | E-GEOD-4710 | biostudies-arrayexpress

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