Transcriptomics of zebrafish cardiac valve regeneration
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA563669 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10060610_1.fastq.gz | Fastqsanger.gz | |||
| SRR10060610_2.fastq.gz | Fastqsanger.gz | |||
| SRR10060611_1.fastq.gz | Fastqsanger.gz | |||
| SRR10060611_2.fastq.gz | Fastqsanger.gz | |||
| SRR10060612_1.fastq.gz | Fastqsanger.gz |
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Project description:Ischemic cardiopathy is the leading cause of death in the world, for which efficient regenerative therapy is not currently available. In mammals, after a myocardial infarction episode, the damaged myocardium is replaced by scar tissue featuring collagen deposition and tissue remodelling with negligible cardiomyocyte proliferation. Zebrafish, in contrast, display an extensive regenerative capacity as they are able to restore completely lost cardiac tissue after partial ventricular amputation. Due to the lack of genetic lineage tracing evidence, it is not yet clear if new cardiomyocytes arise from existing contractile cells or from an uncharacterised set of progenitors cells. Nonetheless, several genes and molecules have been shown to participate in this process, some of them being cardiomyocyte mitogens in vitro. Though questions as what are the early signals that drive the regenerative response and what is the relative role of each cardiac cell in this process still need to be answered, the zebrafish is emerging as a very valuable tool to understand heart regeneration and devise strategies that may be of potential value to treat human cardiac disease. Here, we performed a genome-wide transcriptome profile analysis focusing on the early time points of zebrafish heart regeneration and compared our results with those of previously published data. Our analyses confirmed the differential expression of several transcripts, and identified additional genes the expression of which is differentially regulated during zebrafish heart regeneration. We validated the microarray data by conventional and/or quantitative RT-PCR. For a subset of these genes, their expression pattern was analyzed by in situ hybridization and shown to be upregulated in the regenerating area of the heart. The specific role of these new transcripts during zebrafish heart regeneration was further investigated ex vivo using primary cultures of zebrafish cardiomyocytes and/or epicardial cells. Our results offer new insights into the biology of heart regeneration in the zebrafish and, together with future experiments in mammals, may be of potential interest for clinical applications. In order to study zebrafish heart regeneration, a time course experiment was realized where amputated heart regenerating were compared to control heart. Samples in triplicate were extracted at 1, 3, 5 and 7 days post-amputation.
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Project description:Zebrafish have a high capacity to regenerate their hearts post-injury.Several studies have surveyed transcriptional enhancers to understand how the dynamics of gene expression are controlled during heart regeneration. We have identified a cardiac transcriptional enhancer that is activated at the site of injury called the runx1 enhancer or REN since it regulates the expression of nearby gene runx1. REN is usually active in cardiomyocytes (CMs) and epicardial tissues surrounding the cardiac valves of uninjured zebrafish hearts. However, when REN is activated in regenerating CM and epicardial tissues at the injury site, it is concurrently downregulated around the distal heart valve. Deletion of REN (ΔREN) results in excess Collagen around uninjured zebrafish cardiac valves. This ΔREN Collagen phenotype is rescued with a runx1 deletion (Δrunx1), suggesting that REN and runx1 function in different genetic pathways in uninjured hearts. A different nearby gene that does change expression around valves in ΔREN mutant hearts is adamts1 which encodes a metalloproteinase that degrades Collagen. Taken together, this suggests that in uninjured hearts REN regulates adamts1 independently of runx1. However, during regeneration, CM proliferation at the site of injury is enhanced in both ΔREN and Δrunx1 mutants, suggesting that REN is rewired to runx1 to stimulate its transcription. There are two previous descriptions for how enhancers are activated during regeneration. First, cis-regulatory sequences are reactivated from embryogenesis and second that active adult enhancers are further invigorated during regeneration. Our data point to a third and previously unappreciated mechanism for gene control during zebrafish heart regeneration. We report that an enhancer is repurposed both from one gene and cardiac domain to activate a different nearby gene in regenerating cardiac tissue.
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