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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

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			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

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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

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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.

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Endocardial HAND2 orchestrates hypoxic and TGFbeta signaling to modulate coronary artery formation

Project description:The endocardium is a major source of coronary angiogenesis and arterialization, through coordinated cell fate transition and migration. However, the transcriptional regulatory network synchronizing cell fate determination and movement remains unclear. Here, we identified transcription factor HAND2 as a key candidate for coronary vascular formation. Endocardial deletion of Hand2 in mice disrupted arterial-venous networks and stunted coronary arteries, paralleling a ventricular noncompaction phenotype. Moreover, deletion of Hand2 produced excessive tip cells with defective movement. RNA-seq analysis revealed enhanced hypoxic metabolic activation but declined TGF-β/p38MAPK-dependent Endo-MT. In consistence, genetic inhibition of the core hypoxic regulators or pharmaceutical administration of TGFβ2 partially recovered the coronary arterial defects in Hand2 mutants. Furthermore, HAND2 was found directly bound to promoters of the target genes, harmonizing cell migration and cell fate transition. These findings pinpoint HAND2 as an essential regulator to regulate endocardial transcriptional regulatory network for coronary arterialization and provide potential therapeutic targets for coronary artery diseases.

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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.

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Endocardial HAND2 orchestrates hypoxic and TGFbeta signaling to modulate coronary artery formation [scRNA-seq]

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Endocardial HAND2 orchestrates hypoxic and TGFbeta signaling to modulate coronary artery formation [RNA-Seq]

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Endocardial HAND2 orchestrates hypoxic and TGFbeta signaling to modulate coronary artery formation [CUT&Tag]

Project description:The endocardium is a major source of coronary angiogenesis and arterialization, through coordinated cell fate transition and migration. However, the transcriptional regulatory network synchronizing cell fate determination and movement remains unclear. Here, we identified transcription factor HAND2 as a key candidate for coronary vascular formation. Endocardial deletion of Hand2 in mice disrupted arterial-venous networks and stunted coronary arteries, paralleling a ventricular noncompaction phenotype. Moreover, deletion of Hand2 produced excessive tip cells with defective movement. RNA-seq analysis revealed enhanced hypoxic metabolic activation but declined TGF-β/p38MAPK-dependent EndoMT. In consistence, genetic inhibition of the core hypoxic regulators or pharmaceutical administration of TGFβ2 effectively reversed the coronary arterial defects in Hand2 mutants. Furthermore, HAND2 was found directly bound to promoters of the target genes, harmonizing cell migration and cell fate transition. These findings pinpoint a HAND2-governed endocardial transcriptional regulatory network for coronary arterialization and provide potential therapeutic targets for coronary artery diseases.

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