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

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

PROVIDER: PRJNA733034 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14663897_1.fastq.gz	Fastqsanger.gz
	SRR14663897_2.fastq.gz	Fastqsanger.gz
	SRR14663898_1.fastq.gz	Fastqsanger.gz
	SRR14663898_2.fastq.gz	Fastqsanger.gz

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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

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

Project description:AimsNon-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. We aimed to identify candidate angiocrines expressed by endocardial and endothelial cells (ECs) in wildtype and LVNC conditions in Tie2Cre;Ino80fl/fltransgenic embryonic mouse hearts, and test the effect of these candidates on cardiomyocyte proliferation and maturation.Methods and resultsWe 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, downregulated by Ino80-deficiency, that functioned to promote cardiomyocyte proliferation. Furthermore, mutant endocardial and endothelial cells up-regulated expression of secreted factors, such as Tgfbi, Igfbp3, Isg15, and Adm, which decreased cardiomyocyte proliferation and increased maturation.ConclusionsThese findings support a model where coronary endothelial cells normally promote myocardial compaction through secreted factors, but that endocardial and endothelial cells can secrete factors that contribute to non-compaction under pathological conditions.

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Epicardium Regulates Ventricular Compaction

Project description:Epicardium Regulates Ventricular Compaction

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Epicardium Regulates Ventricular Compaction

Project description:We used single nucleus RNA sequencing (snRNAseq) to show that Numb and Numblike specific deletion in epicardium regulates ventricular compaction via the Numb Family Proteins-Fgf Signaling

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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.

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Sequential Notch activation regulates ventricular chamber development

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Gene expression analysis from bulk RNA isolated from embryonic mouse hearts at time points E13.5 and E14.5 with and without disruption of endothelial Ino80

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Prerequisite endocardial-mesenchymal transition for cardiac trabecular angiogenesis

Project description:We used single cell RNA sequencing (scRNAseq) to show that ventricular endocardial cells generate trabecular vessels through an angioEMT mechanism.

2023-03-07 | GSE205394 | GEO

Transcriptome of embryonic hearts with cardiomyocyte-specific deficiency of Aars2

Project description:We generated cardiomyocyte-specific Aars2 knockout mice, and observed ventricular non-compaction defects and abnormal cardiac morphogenesis at E16.5. All homozygous mutant mice died before birth. We sought to identify the transcriptome changes at E16.5 by Aars2-deficiency in cardiomyocytes.

2026-02-20 | GSE279006 | GEO

The Right Ventricular Fibroblast Secretome Drives Cardiomyocyte Dedifferentiation

Project description:The Right Ventricular Fibroblast Secretome Drives Cardiomyocyte Dedifferentiation

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