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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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Transcriptional profiling of purified endocardial and coronary vascular endothelial cells, isolated from murine embryonic hearts, at two 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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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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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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Single cell evaluation of endocardial HAND2 gene regulatory networks reveals critical HAND2 dependent pathways impacting cardiac morphogenesis.

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