Project description:To investigate the microRNA regulated in the endocardial cells, we performed high-throughput profiling analysis using small RNA-Seq data obtained from Hdac3 CRISPR knockout mouse cardiac endothelail cells

2024-03-20 | GSE229659 | GEO

Endocardial HDAC3 is required for myocardial trabeculation [bulk RNA-seq]

Project description:To investigate the growth factors regulated in the endocardial cells, we performed gene expression profiling analysis using RNA-Seq data obtained from Hdac3 CRISPR knockout mouse cardiac endothelail cells

2024-03-20 | GSE229677 | GEO

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.

2019-05-07 | GSE130741 | GEO

Tie2 regulates endocardial sprouting and myocardial trabeculation

Project description:Tie2 regulates endocardial sprouting and myocardial trabeculation

| PRJNA541264 | ENA

Endocardial HDAC3 is required for myocardial trabeculation [single-cell RNA-seq]

Project description:To investigate the signal communication from the endocardium to the trabecular myocardium, we performed single cell RNA sequencing (scRNA-seq) in E11.5 Hdac3 Tie2 knockout hearts and littermate control hearts

2024-03-20 | GSE229660 | GEO

Endocardial HDAC3 is required for myocardial trabeculation

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-03-20 | GSE229661 | GEO

Myocardial Differentiation is Dependent upon Endocardial Signalling During Early Cardiogenesis in vitro

Project description:The endocardium interacts with the myocardium to promote proliferation and morphogenesis during the later stages of heart development. However, the role of the endocardium in early cardiac ontogeny remains under-explored. Given the shared origin, subsequent juxtaposition, and essential cell-cell interactions of endocardial and myocardial cells throughout heart development, we hypothesized that paracrine signaling from the endocardium to the myocardium is critical for initiating early differentiation of myocardial cells. To test this, we generated an in vitro, endocardial-specific ablation model using the diphtheria toxin receptor under the regulatory elements of the NFATc1 genomic locus (NFATc1-DTR) Early treatment of NFATc1-DTR embryoid bodies with diphtheria toxin efficiently ablated endocardial cells, which significantly attenuated the percent of beating EBs in culture and expression of early and late myocardial differentiation markers. The addition of Bmp2 during endocardial ablation partially rescued myocyte differentiation, maturation and function. Therefore, we conclude that early stages of myocardial differentiation rely on endocardial paracrine signaling mediated in part by Bmp2. Our findings provide novel insight into early endocardial-myocardial interactions that can be explored to promote early myocardial development and growth.

2019-05-01 | GSE119505 | GEO

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