Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA sequencing of secondary heart field- and cardiac neural crest-derived cells from murine aortas

ABSTRACT: RNA sequencing of secondary heart field- and cardiac neural crest-derived cells from murine aortas

PROVIDER: PRJNA783359 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17035319_1.fastq.gz	Fastqsanger.gz
	SRR17035319_2.fastq.gz	Fastqsanger.gz
	SRR17035320_1.fastq.gz	Fastqsanger.gz
	SRR17035320_2.fastq.gz	Fastqsanger.gz
	SRR17035321_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

RNA sequencing of secondary heart field- and cardiac neural crest-derived cells from murine aortas

Project description:To better understand the role of lineage in smooth muscle cell heterogenity along the length of the aorta, we performed bulk RNA-sequencing transcriptomic analysis on secondary heart field (SHF)-derived and cardiac neural crest derived (CNC)-derived sorted cells from murine aortas.

2022-03-14 | GSE189544 | GEO

Neural crest cell derived DKK1 modulates Wnt signalling in the second heart field to orchestrate cardiac outflow tract development.

Project description:Heart morphogenesis is highly complex, and depends on the generation of diverse cell types which interact with each other in an orchestrated manner to remodel the primitive heart tube into a functional organ. Cardiac outflow tract formation critically depends on continued contribution of cardiac progenitor cells from the anterior second heart field to ensure proper growth of the outflow tract. Prior to entering the outflow tract, neural crest cells migrate in close apposition to the second heart field and may play important roles in regulating second heart field growth dynamics, however the molecular mechanisms by which neural crest cells interact with the second heart field have remained elusive. Here, we discover that neural crest cells are a primary source of Dickkopf1 (DKK1), a secreted Wnt signalling inhibitor, which modulates Wnt signalling activity in the second heart field to impose a balance between progenitor maintenance and differentiation. Further, we identify the ubiquitin ligase NEDD4 as a critical regulator of DKK1 levels, with disruption of Nedd4 activity leading to outflow tract defects. In the context of disease pathogenicity, we show a novel human congenital heart disease variant of NEDD4 has lost the ability to ubiquitinate DKK1, and is associated with heart defects in a mouse model of the genetic variant. Our findings point to an unexpected role for neural crest cells acting as a rheostat of Wnt signalling activity in cardiac progenitors, identifying a new molecular pathway underpinning correct outflow tract morphogenesis, and a new causative factor of congenital heart disease.

2025-12-15 | GSE309818 | GEO

Heterogeneous Cardiac- and Neural Crest-Derived Aortic Smooth Muscle Cells have Similar Transcriptional Changes after TGFβ Signaling Disruption [Bulk-RNA-seq-of-Human-aortas]

Project description:We report bulk RNA-seq data of different segments of human thoracic aortas

2025-02-27 | GSE253932 | GEO

Reactivation of an Embryonic Cardiac Neural Crest Transcriptional Subcircuit During Zebrafish Heart Regeneration [scRNA-seq]

Project description:During vertebrate development, the heart primarily arises from mesoderm, with crucial contributions from cardiac neural crest cells that migrate to the heart and form a variety of cardiovascular derivatives. Here, by integrating bulk and single cell RNAseq with ATAC-seq, we identify a gene regulatory subcircuit specific to migratory cardiac crest cells composed of key transcription factors egr1, sox9a, tfap2a and ets1. Notably, we show that cells expressing the canonical neural crest gene sox10 are essential for proper cardiac regeneration in adult zebrafish. Furthermore, expression of all transcription factors from the migratory cardiac crest gene subcircuit are reactivated after injury at the wound edge. Together, our results uncover a developmental gene regulatory network that is important for cardiac neural crest fate determination, with key factors re-activated during regeneration.

2025-01-30 | GSE287811 | GEO

The Secondary Crest Myofibroblast PDGFRa Controls Elastogenesis Pathway via a Secondary Tier of Signaling Networks During Alveogenesis

Project description:To compare the gene expression profiles between normal and Pdgfra deficient secondary crest myofibroblasts (SCMF). There was a total of 1808 differentially expressed genes of which 866 increased, while 942 decreased in the Pdgfra deficient SCMFs. The differentially expressed genes are related to multiple functions of SCMFs. Pdgfra plays an important role in multiple functions, especially elastogenesis, of secondary crest myofibroblasts during alveolar formation.

2019-02-13 | GSE126457 | GEO

Reactivation of an Embryonic Cardiac Neural Crest Transcriptional Subcircuit During Zebrafish Heart Regeneration [bulk RNA-seq]

2025-01-30 | GSE287815 | GEO

Reactivation of an Embryonic Cardiac Neural Crest Transcriptional Subcircuit During Zebrafish Heart Regeneration [bulk ATAC-seq]

2025-01-30 | GSE287813 | GEO

Endothelial cells regulate neural crest and second heart field morphogenesis.

Project description:Cardiac and craniofacial developmental programs are intricately linked during early embryogenesis, which is also reflected by a high frequency of birth defects affecting both regions. The molecular nature of the crosstalk between mesoderm and neural crest progenitors and the involvement of endothelial cells within the cardio-craniofacial field are largely unclear. Here we show in the mouse that genetic ablation of vascular endothelial growth factor receptor 2 (Flk1) in the mesoderm results in early embryonic lethality, severe deformation of the cardio-craniofacial field, lack of endothelial cells and a poorly formed vascular system. We provide evidence that endothelial cells are required for migration and survival of cranial neural crest cells and consequently for the deployment of second heart field progenitors into the cardiac outflow tract. Insights into the molecular mechanisms reveal marked reduction in Transforming growth factor beta 1 (Tgfb1) along with changes in the extracellular matrix (ECM) composition. Our collective findings in both mouse and avian models suggest that endothelial cells coordinate cardio-craniofacial morphogenesis, in part via a conserved signaling circuit regulating ECM remodeling by Tgfb1.

| S-EPMC4133721 | biostudies-literature

Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

Project description:Neural crest defects lead to congenital heart disease involving outflow tract (OFT) malformation. Integrin-linked-Kinase (ILK) plays important roles in multiple cellular processes and embryogenesis. ILK is expressed in neural crest cells (NCC), but its role in NCC and OFT morphogenesis remains unknown. We used microarrays to detail the global programme of gene expression underlying the morphogenesis of the cardiac neural crest and outflow tract. The outflow tract of control and ILK mutant mouse embryos at E10.5 were dissected and dissociated. Neural crest cells were FACS sorted and used for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-01 | E-GEOD-41179 | biostudies-arrayexpress

Cardiac Neural Crest.

Project description:Cardiac neural crest (CNC) cells are pluripotent cells derived from the dorsal neural tube that migrate and contribute to the remodeling of pharyngeal arch arteries and septation of the cardiac outflow tract (OFT). Numerous molecular cascades regulate the induction, specification, delamination, and migration of the CNC. Extensive analyses of the CNC ranging from chick ablation models to molecular biology studies have explored the mechanisms of heart development and disease, particularly involving the OFT and aortic arch (AA) system. Recent studies focus more on reciprocal signaling between the CNC and cells originated from the second heart field (SHF), which are essential for the development of the OFT myocardium, providing new insights into the molecular mechanisms underlying congenital heart diseases (CHDs) and some human syndromes.

| S-EPMC7778148 | biostudies-literature

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