Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Endocardial Notch Signaling Promotes Cardiomyocyte Proliferation in the Regenerating Zebrafish Heart through Wnt Pathway Antagonism

ABSTRACT: Endocardial Notch Signaling Promotes Cardiomyocyte Proliferation in the Regenerating Zebrafish Heart through Wnt Pathway Antagonism

PROVIDER: PRJNA419372 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6313720_1.fastq.gz	Fastqsanger.gz
	SRR6313720_2.fastq.gz	Fastqsanger.gz
	SRR6313721_1.fastq.gz	Fastqsanger.gz
	SRR6313721_2.fastq.gz	Fastqsanger.gz
	SRR6313722_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Endocardial Notch Signaling Promotes Cardiomyocyte Proliferation in the Regenerating Zebrafish Heart through Wnt Pathway Antagonism

Project description:The goal of this study is to understand the molecular mechanisms underlying this Notch-induced muscle cell proliferation defect, we sequenced the transcriptome of control ventricles and Notch-suppressed ventricle at 5 days post-injury, when cardiomyocyte proliferation is normally robust.

2019-01-01 | GSE107228 | GEO

Endocardial Notch Signaling Promotes Cardiomyocyte Proliferation in the Regenerating Zebrafish Heart through Wnt Pathway Antagonism.

Project description:Previous studies demonstrate that the regenerative zebrafish heart responds to injury by upregulating Notch receptors in the endocardium and epicardium. Moreover, global suppression of Notch activity following injury impairs cardiomyocyte proliferation and induces scarring. However, the lineage-specific requirements for Notch signaling and full array of downstream targets remain unidentified. Here, we demonstrate that inhibition of endocardial Notch signaling following ventricular amputation compromises cardiomyocyte proliferation and stimulates fibrosis. RNA sequencing uncovered reduced levels of two transcripts encoding secreted Wnt antagonists, Wif1 and Notum1b, in Notch-suppressed hearts. Like Notch receptors, wif1 and notum1b are induced following injury in the endocardium and epicardium. Small-molecule-mediated activation of Wnt signaling is sufficient to impair cardiomyocyte proliferation and induce scarring. Last, Wnt pathway suppression partially restored cardiomyocyte proliferation in hearts experiencing endocardial Notch inhibition. Taken together, our data demonstrate that Notch signaling supports cardiomyocyte proliferation by dampening myocardial Wnt activity during zebrafish heart regeneration.

| S-EPMC6366857 | biostudies-literature

Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of ventricular non-compaction

Project description:Non-compaction cardiomyopathy is a devastating genetic disease caused by insufficient consolidation of ventricular wall muscle that can result in inadequate cardiac performance. Despite being the third most common cardiomyopathy, the mechanisms underlying the disease, including the cell types involved, are poorly understood. We have previously shown that endothelial cell-specific deletion of the chromatin remodeller gene Ino80 results in defective coronary vessel development that leads to ventricular non-compaction in embryonic mouse hearts. Here, we used single-cell RNA-sequencing to characterize endothelial and endocardial defects in Ino80-deficient hearts. We observed a pathological endocardial cell population in the non-compacted hearts and identified multiple dysregulated angiocrine factors that dramatically affected cardiomyocyte behaviour. We identified Col15A1 as a coronary vessel-secreted angiocrine factor, down-regulated by Ino80-deficiency, which functioned to promote cardiomyocyte proliferation. Furthermore, mutant endocardial and endothelial cells (ECs) AQ6 up-regulated expression of secreted factors, such as Tgfbi, Igfbp3, Isg15, and Adm, which decreased cardiomyocyte proliferation and increased maturation. These findings support a model where coronary ECs normally promote myocardial compaction through secreted factors, but that endocardial and ECs can secrete factors that contribute to non-compaction under pathological conditions.

2021-12-30 | GSE175589 | GEO

Tie2 regulates endocardial sprouting and myocardial trabeculation

Project description:The ang1-Tie2 pathway is required for normal vascular development, but its molecular effectors are not well-defined during cardiac ontogeny. Here we show that endocardial specific attenuation of Tie2 results in mid-gestation lethality due to heart defects associated with a hyperplastic but simplified trabecular meshwork (fewer but thicker trabeculae). Reduced proliferation and production of endocardial cells (ECs) following endocardial loss of Tie2 results in decreased endocardial sprouting required for trabecular assembly and extension. The hyperplastic trabeculae result from enhanced proliferation of trabecular cardiomyocyte (CMs), which is associated with upregulation of Bmp10, increased retinoic acid (RA) signaling, and Erk1/2 hyperphosphorylation in the myocardium. Intriguingly, myocardial phenotypes in Tie2-cko hearts could be partially rescued by inhibiting in utero RA signaling with pan-retinoic acid receptor antagonist BMS493. These findings reveal two complimentary functions of endocardial Tie2 during ventricular chamber formation: ensuring normal trabeculation by supporting EC proliferation and sprouting, and preventing hypertrabeculation via suppression of RA signaling in trabecular CMs.

2019-05-07 | GSE130741 | GEO

Regenerating axolotl retinas regrow diverse cell types with modulation by Notch signaling and reconnect to the brain

Project description:We examined uninjured and regenerating axolotl salamander retinas, including their transcriptional profile. We report that at 27 days after a retinectomy (early-mid regeneration), regenerating axolotl retinas exhibit downregulation of genes associated with neuronal networks but upregulation of genes associated with angiogenesis and the extracellular matrix. We also report differential expression of two Notch pathway effector genes, Hes1 and Hes5.

2022-04-10 | GSE200423 | GEO

Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

| PRJNA928078 | ENA

Exercise in adult zebrafish promotes ventricular cardiomyocyte proliferation in the regenerating heart

Project description:Exercise promotes a set of physiological adaptations known to provide long-term health benefits and it can play an important role in cardioprotection. However, the mechanisms underlying exercise-induced cardiac adaptation are not fully understood. In the present study, we examined cardiac adaptive responses to exercise training in the adult zebrafish and in the context of cardiac regeneration.We found that swimming-induced exercise increased cardiomyocyte proliferation and that this response was also found under regenerating conditions, when exercise was performed either prior to and after ventricular cryoinjury (CI). Exercise prior to CI resulted in a mild improvement in cardiac function and lesion recovery over the non-exercise condition.Transcriptomic profiling of regenerating ventricles in cryoinjured fish subjected to exercise revealed a differential regulation of genes related toregeneration as well as other biological processes potentially involved in the exercise response. Taken together, these results suggest that exercise constitutes a physiological stimulus thatmay help promote cardiomiogenic mechanisms of the vertebrate heart and that the zebrafish exercise model may be useful for evaluating the potential cardioprotective effects of exercise.

2018-10-18 | GSE100892 | GEO

Single-Cell RNA-Seq and Patient-Specific iPSCs Reveal Endocardial Abnormalities in Hypoplastic Left Heart Syndrome

Project description:Hypoplastic left heart syndrome (HLHS) is one of the most devastating forms of congenital heart defects. Previous studies have only focused on intrinsic defects in the myocardium. However, this does not sufficiently explain the abnormal development of the cardiac valve, septum, and vasculature, which are known to originate from the endocardium. Here, using single-cell RNA profiling, induced pluripotent stem cells, and fetal heart tissue with an underdeveloped left ventricle, we identified a developmentally impaired endocardial cell population in HLHS. The intrinsic endocardial deficits contributed to abnormal endothelial to mesenchymal transition, NOTCH signaling, and extracellular matrix organization, all of which are key factors in valve formation. Consequentially, endocardial abnormalities conferred reduced proliferation and maturation of cardiomyocytes through a disrupted fibronectin-integrin interaction. Several known HLHS de novo mutations all contributed to the abnormal endocardial gene expression through the alteration of promoter/enhancer activities. These mechanistic discoveries provide an alternative angle for early intervention and heart regeneration in HLHS.

2020-08-17 | GSE138979 | GEO

Endocardial cells function as antigen-presenting cells to promote zebrafish heart regeneration

Project description:In contrast to adult mammals, adult zebrafish are able to fully regenerate injured cardiac tissue, and this regeneration process requires an adequate and tightly controlled immune response. However, which immune aspects drive particular aspects of the regenerative response are unclear. Here, we report the participation and requirement of the antigen presentation-adaptive immunity axis during zebrafish cardiac regeneration. We found that, in addition to immune cells, endocardial cells start expressing antigen presentation genes following the initial innate immune response. Consistent with this finding, we observed that helper T cells, a.k.a. Cd4+ T cells, are closely associated with phosphoERK+ (pERK+) (i.e., activated) endocardial cells at these stages. We inactivated major histocompatibility complex (MHC) class II antigen presentation by generating cd74a; cd74b double mutants, which display a defective immune response. In these mutants, both Cd4+ T cells and pERK+ endocardial cells fail to efficiently infiltrate the injured tissue. Notably, this model of compromised antigen presentation exhibits additional defects in cardiac regeneration including reduced cardiomyocyte dedifferentiation and proliferation. Altogether, these findings reveal a necessary role for antigen presentation during zebrafish cardiac regeneration and point to an immune crosstalk between T cells and endocardial cells, thereby further establishing a link between the adaptive immune response and tissue regeneration.

2024-03-06 | GSE230669 | GEO

Label-free quantitative Proteomics Analysis Reveals Distinct Molecular characteristics in Endocardial Endothelium

Project description:Endocardial endothelium, which lines the chambers of the heart, is distinct in its origin, structure, and function. However, though functionally very important, no studies at protein level have been conducted so far characterizing endocardial endothelium. In this study, we used endothelial cells from pig heart to investigate if endocardial endothelial cells are distinct at the proteome level. Using a high throughput liquid chromatography-tandem mass spectrometry for proteome profiling and expression, we identified sets of proteins that belong to specific biological processes and metabolic pathways in endocardial endothelial cells supporting its specific structural and functional roles.

2018-06-29 | PXD009194 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data