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Single cell evaluation of endocardial HAND2 gene regulatory networks reveals critical HAND2 dependent pathways impacting cardiac morphogenesis.

ABSTRACT: Single cell evaluation of endocardial HAND2 gene regulatory networks reveals critical HAND2 dependent pathways impacting cardiac morphogenesis.

PROVIDER: PRJNA864790 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20731048.fastq.gz	Fastqsanger.gz
	SRR20731049.fastq.gz	Fastqsanger.gz
	SRR20731050.fastq.gz	Fastqsanger.gz
	SRR20731051.fastq.gz	Fastqsanger.gz

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Single cell evaluation of endocardial HAND2 gene regulatory networks reveals critical HAND2 dependent pathways impacting cardiac morphogenesis.

Project description:The basic-helix-loop-helix transcription factor HAND2 plays a critical role in endocardium to myocardium signaling during cardiac morphogenesis through its role within the NOTCH signaling pathway. Hand2 endocardial deletion (H2CKOs) results in embryonic lethality by E13.5 due to tricuspid atresia (TA) or double inlet left ventricle (DILV) with accompanying intraventricular septum defects, multiple septa, and hypo-trabeculated ventricles. In addition, H2CKOs also exhibit an increased density of coronary lumens. In order to understand the underlying regulatory mechanisms that cause these phenotypes, we undertook a single cell transcriptome analysis of E11.5 H2CKOs hearts.

2023-01-09 | GSE210221 | GEO

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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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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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]

2026-05-31 | GSE311982 | GEO

Single cell evaluation of endocardial Hand2 gene regulatory networks reveals HAND2-dependent pathways that impact cardiac morphogenesis.

Project description: Not available

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Transcription profile of zebrafish hand2 (hanS6 allele) mutant embryos at 19hpf

Project description:Heart formation requires the fusion of bilateral cardiomyocyte populations as they move toward the embryonic midline. The bHLH transcription factor Hand2 is essential for cardiac fusion; however, the effector genes that execute this function of Hand2 are unknown. Here, we provide the first evidence for a downstream component of the Hand2 pathway that mediates cardiac morphogenesis. Although hand2 is expressed in cardiomyocytes, mosaic analysis demonstrates that hand2 plays a non-autonomous role in regulating cardiomyocyte movement. Gene expression profiles reveal heightened expression of fibronectin 1 (fn1) in hand2 mutant embryos. Reciprocally, overexpression of hand2 leads to decreased Fibronectin levels. Furthermore, reduction of fn1 function enables rescue of cardiac fusion in hand2 mutants: bilateral cardiomyocyte populations merge and exhibit improved tissue architecture, albeit without major changes in apicobasal polarity. Together, our data provide a novel example of a tissue creating a favorable environment for its morphogenesis: the Hand2 pathway establishes an appropriate environment for cardiac fusion through negative modulation of Fn1 levels. Embryos from three independent hand2 mutant (hanS6 allele) heterozyogous crosses were collected. Examination of Tg(myl7:egfp) expression allow sorting of hand2 mutant embryos from their wild-type siblings.

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

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

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Transcription profile of zebrafish hand2 (hanS6 allele) mutant embryos at 19hpf

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

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

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