Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling of purified endocardial and coronary vascular endothelial cells, isolated from murine embryonic hearts, at two developmental stages

ABSTRACT: Transcriptional profiling of purified endocardial and coronary vascular endothelial cells, isolated from murine embryonic hearts, at two developmental stages

PROVIDER: PRJNA613061 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11336106.fastq.gz	Fastqsanger.gz
	SRR11336107.fastq.gz	Fastqsanger.gz
	SRR11336108.fastq.gz	Fastqsanger.gz
	SRR11336109.fastq.gz	Fastqsanger.gz
	SRR11336110.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Transcriptional profiling of purified endocardial and coronary vascular endothelial cells, isolated from murine embryonic hearts, at two developmental stages

Project description:Given that the Nes-gfp allele specifically labels coronary ECs, endogenous GFP and the endomucin marker (which was highly expressed in endocardial cells) were used together to separate endocardial and coronary vascular endothelial cell subpopulations in different developmental stages

2021-02-20 | GSE147117 | GEO

Transcriptional profiling of endocardial and (arterial or venous-enriched) coronary vascular endothelial cells, purified from murine embryonic hearts at E17.5.

Project description:Transcriptional profiling of endocardial and (arterial or venous-enriched) coronary vascular endothelial cells, purified from murine embryonic hearts at E17.5.

| PRJNA613050 | ENA

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

Transcriptional profiling of endocardial and (arterial or venous-enriched) coronary vascular endothelial cells, purified from murine embryonic hearts at E17.5.

Project description:A specific tracing system, selectively labeling tomato+ intramyocardial vessels with the Nes-CreER driver, was used together with the Nes-Gfp reporter and endomucin marker to separate, from the same hearts, the three subsets of Ecs (ventricular endocardium, intramyocardial arterial-enriched, and subepicardial venous-enriched endothelial cells), which were subject to transcriptome profiling by RNASeq.

2021-02-20 | GSE147108 | GEO

Endocardium-to-coronary artery differentiation during heart development and regeneration involves sequential roles of Bmp2 and Cxcl12/Cxcr4.

Project description:Endocardial cells lining the heart lumen are coronary vessel progenitors during embryogenesis. Re-igniting this developmental process in adults could regenerate blood vessels lost during cardiac injury, but this requires additional knowledge on molecular regulators. Here, we use mouse genetics and scRNAseq to identify novel regulators of endocardial angiogenesis and precisely assess the role of CXCL12/CXCR4 signaling. Time-specific lineage tracing demonstrated that endocardial cells differentiated in coronary endothelial cells primarily at mid-gestation. A new mouse line reporting CXCR4 activity—along with cell-specific gene deletions—revealed it was specifically required for artery morphogenesis rather than angiogenesis. Integrating scRNAseq data of endocardial-derived coronary vessels from mid- and late-gestation identified a Bmp2-expressing transitioning population specific to mid-gestation. Bmp2 stimulated endocardial angiogenesis in vitro and in injured neonatal mouse hearts. Our data shed light on how understanding the molecular mechanisms underlying endocardial angiogenesis can identify new potential therapeutic targets promoting revascularization of the injured heart.

2022-10-09 | GSE214942 | GEO

Single cell transcriptional profiles of endothelial cells sorted from the hearts with ablation of Wnt/beta-catenin signaling activating cardiomyocytes and without ablation [scRNA-seq]

Project description:To understand how Wnt/β-catenin signaling-activated cardiomyocytes (β-cat ON CMs) promote coronary vessel development, we performed single-cell RNA sequencing of endothelial cells (ECs) sorted from the hearts ablated β-cat ON CMs and those from control hearts, respectively. Our analyses indicated that β-cat ON CMs regulates coronary vessel development by promoting arterialization, a step in the transition of endocardial ECs to coronary ECs.

2024-08-23 | GSE223461 | GEO

Gene expression analysis of control and Tbx20 mutant Tie2Cre lineage from E12.5 hearts

Project description:To investigate roles for Tbx20 in endocardium, we ablated Tbx20 utilizing Tie2Cre. Tie2Cre;Tbx20 mutants died at E14, exhibiting defects in multiple aspects of cardiac septation. Although endocardial cells lacking Tbx20 were able to undergo endothelial-to-mesenchymal transition, cushion mesenchymal cells lacking Tbx20 did not disperse normally. Non-cell autonomous roles of endocardial Tbx20 were also revealed, as evidenced by decreased myocardialization of outflow tract and failure of dorsal mesenchymal protrusion formation in mutants. To examine how ablation of Tbx20 in endocardial lineages affected gene expression, we performed global gene expression analysis on purified endocardial lineages. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+). Mutant endocardial lineages exhibited decreased expression of genes associated with extracellular matrix and cell migration. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+). FACS sorted Tie2Cre lineage from E12.5 hearts: Tie2Cre;Tbx20 +/loxP Control hearts versus Tie2Cre;Tbx20 loxP/- mutant hearts

2016-07-01 | E-GEOD-73858 | biostudies-arrayexpress

Molecular classification of failing hearts from coronary and myopathic patients

Project description:RNA form the heart a goupe of 9 patients with end stage cardiomyopathy (CAD) and 11 patiensts with coronary artery disease (CAD) was hybridized against pooled RNA form 4 normal nonfailing hearts.

2010-06-06 | E-GEOD-2014 | biostudies-arrayexpress

Molecular classification of failing hearts from coronary and myopathic patients

2005-11-24 | GSE2014 | GEO

Gene expression analysis of control and Tbx20 mutant Tie2Cre lineage from E12.5 hearts

2016-07-01 | GSE73858 | GEO