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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Telomerase is essential for zebrafish heart regeneration

ABSTRACT: Unlike human hearts, zebrafish hearts efficiently regenerate after injury. Regeneration is driven by the strong proliferation response of its cardiomyocytes to injury. In this study, we show that active telomerase is required for cardiomyocyte proliferation and full organ recovery, supporting the potential of telomerase therapy as a means of stimulating cell proliferation upon myocardial infarction. Heart transcriptomes of WT and telomerase defective adult zebrafish animals were profiled by RNASeq, in control conditions and 3 days after heart cryoinjury.

ORGANISM(S): Danio rerio

SUBMITTER: Manuel Gomez

PROVIDER: E-GEOD-71755 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Telomerase is essential for zebrafish heart regeneration

Project description:Unlike human hearts, zebrafish hearts efficiently regenerate after injury. Regeneration is driven by the strong proliferation response of its cardiomyocytes to injury. In this study, we show that active telomerase is required for cardiomyocyte proliferation and full organ recovery, supporting the potential of telomerase therapy as a means of stimulating cell proliferation upon myocardial infarction.

2015-08-06 | GSE71755 | GEO

Evaluating the effects of cardiac telomerase re-activation after myocardial infarction in adult mice

Project description:Coronary heart disease is a main cause of death in the developed world and treatment success remains modest with high mortality rates within one year after myocardial infarction (MI). Thus, new therapeutic targets and effective treatments are necessary. Short telomeres are risk factors for age-associated diseases including heart disease. Here, we address the potential of telomerase (Tert) activation in prevention of heart failure after MI in adult mice. We use adeno-associated viruses for cardiac-specific Tert expression in a mouse model of MI. We find that upon MI, hearts expressing Tert show attenuated cardiac dilation, improved ventricular function and smaller infarct scars concomitant with increased mouse survival by 17% compared to controls. Furthermore, Tert treatment results in elongated telomeres, increased numbers of Ki67 and pH3-positive cardiomyocytes and a gene expression switch towards a regeneration signature of neonatal mice. Our work highlights telomerase activation as a novel therapeutic strategy to prevent heart failure after MI. Mice of one year of age were left untreated (control) or injected with 5*10^11 adeno associated viruses particles of serotype 9 (AAV9) that carry either en empty expression cassette or express telomerase under control of the CMV promoter. Virus injected mice then underwent myocardial infarction induced through permenant left anterior descending artery (LAD) ligation. Mice that survived for six weeks after LAD ligation were sacrificed and 4 hearts per group (AAV9-empty or AAV9-Tert) and 3 control hearts (no virus treatment, no ligation) were subjected to total RNA isolation for micro array analysis.

2014-12-15 | E-GEOD-62973 | biostudies-arrayexpress

Amino acid priming of mTOR is essential for heart regeneration

Project description:For a short period of time in mammalian neonates, the mammalian heart can regenerate via cardiomyocyte proliferation. This regenerative capacity is largely absent in adults. In other organisms, including zebrafish, damaged hearts can regenerate throughout their lifespans. Many studies have been performed to understand the mechanisms of cardiomyocyte de-differentiation and proliferation during heart regeneration however, the underlying reason why adult zebrafish and young mammalian cardiomyocytes are primed to enter cell cycle have not been identified. Here we show the primed state of a pro-regenerative cardiomyocyte is dictated by its amino acid profile and metabolic state. Adult zebrafish cardiomyocyte regeneration is a result of amino acid-primed mTOR activation. Zebrafish and neonatal mouse cardiomyocytes display elevated glutamine levels, predisposing them to amino acid-driven activation of mTORC1. Injury initiates Wnt/β-catenin signalling that instigates primed mTORC1 activation, Lin28 expression and metabolic remodeling necessary for zebrafish cardiomyocyte regeneration. These studies reveal a unique mTORC1 primed state in zebrafish and mammalian regeneration competent cardiomyocytes.

2022-02-15 | PXD011791 | Pride

Transcriptome analysis of heart regeneration in adult zebrafish

Project description:After heart injury, adult zebrafish can perfectly regenerate its heart without any scar tissue left. We performed 100bp*2, paired-end, strand-specific, polyA-positive RNA-seq on hearts from 2 group of adult zebrafish, in which one was sham group and the other 7 days after heart tip amputation (7dpa). We found pathways involving hydrogen peroxidate related functions significantly up-regulated in 7dpa group, indicating its role in heart regeneration. RNA-seq: hearts from sham or 7dpa adult zebrafish

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Evaluating the effects of cardiac telomerase re-activation after myocardial infarction in adult mice

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Fine-Tuning of PGC1α Expression Regulates Cardiac Function and Longevity (RNA-seq: telomerase-deficient vs PGC1aOE)

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2022-08-01 | GSE135404 | GEO

Midkine-a regulates the formation of a fibrotic scar during zebrafish heart regeneration

Project description:Midkine-a is a cytokine that is highly expressed in the heart upon injury that its role in regeneration has not been identified. We generated a KO zebrafish lines, mdkacn105, and studied the effect of mdka deletion in zebrafish adult heart regeneration. By combining histology and high-throughput genomics, we found that loss of mdka leads to arrest of heart regeneration. Mdka mutant hearts display increased collagen deposition in the site of the injury and decreased proliferation of the coronary endothelial cells due to increased expression of ECM including collagen and periostin as well as decreased expression of Hif1a. Our results demonstrate the importance of a balanced fibrotic respond is necessary for heart regeneration and indicates mdka importance in this process.

2021-05-26 | GSE166732 | GEO

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

Bulk RNA-seq dataset of uninjured vs injured larval zebrafish hearts at 48 hours post injury on 5 days post fertilisation

Project description:This experiment sought to understand the transcriptomic changes that occur in the larval zebrafish heart following injury. 600 hearts were laser injured at 3 days post fertilisation, extracted 48 hours later and pooled into three groups of 200. RNA was extracted from the whole heart(s) and sent for sequencing along with 3 groups of 200 uninjured hearts, extracted and processed identically. RNA sequencing, quality control and alignment was performed by the commercial company GENEWIZ.

2021-10-01 | E-MTAB-10860 | biostudies-arrayexpress

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

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