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Fast revascularization of the injured area is essential to support zebrafish heart regeneration

ABSTRACT: To better understand the possible mechanisms that vegfaa mutants display to compensate for the lack of vegfaa, we performed transcriptomic profiling of vegfaa+/+ and vegfaa-/- ventricles. Total RNA was isolated from hearts extracted from vegfaa+/+ and vegfaa-/- fish (8 months old) pooling 4 hearts per sample.

ORGANISM(S): Danio rerio

PROVIDER: GSE78945 | GEO | 2016/09/25

SECONDARY ACCESSION(S): PRJNA314483

REPOSITORIES: GEO

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Fast revascularization of the injured area is essential to support zebrafish heart regeneration.

Project description:Zebrafish have a remarkable capacity to regenerate their heart. Efficient replenishment of lost tissues requires the activation of different cell types including the epicardium and endocardium. A complex set of processes is subsequently needed to support cardiomyocyte repopulation. Previous studies have identified important determinants of heart regeneration; however, to date, how revascularization of the damaged area happens remains unknown. Here, we show that angiogenic sprouting into the injured area starts as early as 15 h after injury. To analyze the role of vegfaa in heart regeneration, we used vegfaa mutants rescued to adulthood by vegfaa mRNA injections at the one-cell stage. Surprisingly, vegfaa mutants develop coronaries and revascularize after injury. As a possible explanation for these observations, we find that vegfaa mutant hearts up-regulate the expression of potentially compensating genes. Therefore, to overcome the lack of a revascularization phenotype in vegfaa mutants, we generated fish expressing inducible dominant negative Vegfaa. These fish displayed minimal revascularization of the damaged area. In the absence of fast angiogenic revascularization, cardiomyocyte proliferation did not occur, and the heart failed to regenerate, retaining a fibrotic scar. Hence, our data show that a fast endothelial invasion allows efficient revascularization of the injured area, which is necessary to support replenishment of new tissue and achieve efficient heart regeneration. These findings revisit the model where neovascularization is considered to happen concomitant with the formation of new muscle. Our work also paves the way for future studies designed to understand the molecular mechanisms that regulate fast revascularization.

| S-EPMC5056108 | biostudies-literature

Ribosomal profiling of WT and mORF4/NBDY KO hearts [WT_vs_mORF4-NBDYKO_RNAseq]

Project description:Left ventricles from the hearts of adult WT and mORR4/NBDY KO mice were obtained.

2020-07-27 | GSE155133 | GEO

Characterization of myocardial B cells in naïve hearts, acutely injured hearts and acutely injured hearts of mice treated with Pirfenidone

Project description:Myocardial CD19+CD11b+ and CD19+CD11b- cells were FACS sorted from transgenic mice expressing the Diphtheria Toxin (DT) receptor under the myocardial specific MLC2v promoter. Cells were sorted from hearts of mice not exposed to DT (naïve hearts), from the hearts of animals treated with DT 4 days prior to the experiment (DTR) and from the hearts of mice exposed to DT and fed chow enriched with the anti-inflammatory/anti-fibrotic drug Pirfenidone (0.5% in powdered chow, PFD)

2018-12-25 | GSE112984 | GEO

Gene and exon expression change in cardiac hypertrophy with pressure overload

Project description:Pathological cardiac hypertrophy was induced by pressure overload on the heart. We performed genome-wide exon array experiments with left ventricles of mice with 1 week and 4 week of transverse aortic constriction (TAC). The exon level analysis revealed widespread regulation of alternative splicing and alternative polyadenylation during hypertrophy. Exon and gene expression changes were examined in 1 week and 4 week TAC-operated hearts compared to sham-operated hearts. We used C57/BL6 wildtype mice, and their left ventricles were subject to surgery (each n=2).

2011-05-01 | E-GEOD-24242 | biostudies-arrayexpress

Ribosomal profiling of WT and mORF4/NBDY KO hearts

Project description:Left ventricles from the hearts of adult WT and mORR4/NBDY KO mice were obtained. Per heart, RNA-sequencing and ribosomal profiling was performed on the same heart

2020-07-23 | GSE154940 | GEO

Transcriptome-wide mRNA alterations in Streptozotocin induced Type I diabetic mouse heart

Project description:We sequenced mRNA from Left Ventricles of Streptozotocin induced Type I diabetic mouse hearts or mock treated controls at 4 weeks post-treatment in order to assess alternative splicing changes.

2016-05-26 | GSE80664 | GEO

Differential gene expression analysis of 4days post fertilization (dpf) wildtype and flt1ka601zebrafish mutants to identify venous sprouting associated genes

Project description:Formation of organ-specific vasculatures requires cross-talk between developing tissue and specialized endothelial cells. Here we show how developing zebrafish spinal cord neurons coordinate vessel growth through balancing of neuron-derived Vegfaa, with neuronal sFlt1 restricting Vegfaa-Kdrl mediated angiogenesis at the neurovascular interface. Neuron-specific loss of flt1 or increased neuronal vegfaa expression promotes angiogenesis and peri-neural tube vascular network formation. Combining loss of neuronal flt1 with gain of vegfaa promotes sprout invasion into the neural tube. Upon loss of neuronal flt1, ectopic sprouts emanate from veins involving special angiogenic cell behaviors including nuclear positioning and a molecular signature distinct from primary artery or secondary venous sprouting. Manipulation of AV identity or Notch signaling established that ectopic sprouting in flt1 mutants requires venous endothelium. Conceptually our data suggest that spinal cord vascularization proceeds from veins involving two-tiered regulation of neuronal sFlt1 and Vegfaa via a novel sprouting mode.

2016-11-01 | GSE89350 | GEO

Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction [snRNA-Seq]

Project description:To generate the reference for cell composition deconvolution and characterize the cellular expression landscape, we performed single nucleus RNA-Seq (snRNA-Seq) on left ventricles from four non-failing hearts and one failing heart.

2021-06-04 | GSE161470 | GEO

RNA sequencing on uninjured and injured cardiac regions of B6 and C3H strains

Project description:Purpose: To analyze gene expression in calcific (C3H) and non-calcific (B6) hearts Methods: B6 and C3H mice were induced cardiac injury by rapid freeze thaw of cardiac tissue (cryo-injury). A left thoracotomy was performed at the level of 2nd intercostal space and the exposed beating heart was frozen for 10 seconds by gently pressing a pre-cooled steel rod of 1mm diameter in dry ice. Freezing of cardiac tissue was confirmed by the rapid discoloration of the tissue. Seven days after injury, injured and uninjured regions from same heart were used for RNA sequence. Results: In contrast to only 70 odd genes that were differentially upregulated following injury in non-calcified mouse hearts (B6) about 960 genes were upregulated in C3H hearts following injury induced calcification. Out of the 960 differentially upregulated genes, only 35 were found to be common or upregulated in both C3H and B6 hearts after injury illustrating of the overlapping but dramatically different magnitude of the injury response. Families of genes regulating diverse aspects of an injury response including inflammation, extracellular matrix proteins, cell proliferation and collagen production were differentially expressed between the calcific and non-calcific hearts after injury. The mean expression of osteogenic genes (osteogenic signature) was significantly higher in injured C3H hearts compared to uninjured C3H hearts. The osteogenic signature was not higher in injured B6 hearts compared to control uninjured B6 hearts. Conclusions: Calcific hearts compared to non-calcific hearts responded to injury with a dramatically different transcriptional program.

2016-11-07 | GSE87837 | GEO

Gene expression changes in injured myocardium of Ciona intestinalis

Project description:Ciona intestinalis is an invertebrate animal model system that is well characterized and has many advantages for the study of cardiovascular biology. The regulatory mechanisms of cardiac myocyte proliferation in Ciona are intriguing since Ciona are capable of regeneration throughout their lifespan. To identify important regeneration factors in Ciona, microarray analysis was conducted on RNA from adult Ciona hearts with normal or damaged myocardium using custom Affymetrix GeneChips. After a 24- or 48-hour recovery period, total RNA was isolated from damaged and control hearts. Initial results indicate significant changes in gene expression in hearts damaged by ligation in comparison to cryoinjured or control hearts. Ligation injury shows differential expression of 223 genes as compared to control (fold change >2, p<0.01, Student’s t-test) with limited false discovery (5.8%). Among these 223 genes, 117 have known human orthologs of which 68 were up-regulated and 49 were down-regulated. Notably, FGF 9/16/20 and Ras were significantly upregulated in injured hearts. Histological analyses of injured myocardium were conducted in parallel to the microarray study. Taken together, these studies will coordinate differences in gene expression to cellular changes in the regenerative myocardium of Ciona, which will help to elucidate the regulatory mechanisms of cardiac myocyte proliferation across chordates.

2024-02-06 | GSE244713 | GEO

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