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Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

ABSTRACT: Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

PROVIDER: PRJNA927818 | ENA |

REPOSITORIES: ENA

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Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

Project description:We have manipulated the NOTCH signaling pathway in mouse embryonic endocardial cells by the co-culture with OP9 stromal cells expressing Jag1 and Dll4, the culture over recombinant JAG1 and DLL4, and the use of the γ-secretase inhibitor RO4929097. We have performed RNA-seq and ATAC-seq to define the transcriptional profile and the chromatin accessibility landscape specific for each condition.

2023-12-08 | GSE223735 | GEO

Bmp2 and Notch cooperate to pattern the embryonic endocardium

Project description:Bmp2 and Notch cooperate to pattern the embryonic endocardium

| PRJNA413427 | ENA

Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

| PRJNA928078 | ENA

Bmp2 and Notch cooperate to pattern the embryonic endocardium

Project description:Our study describes in detail the role of Bmp2 during cardiac valve developmnent and its implication in Notch pathway activation.

2018-06-14 | GSE104670 | GEO

Vismodegib and Gamma-Secretase/Notch Signalling Pathway Inhibitor RO4929097 in Treating Patients With Advanced or Metastatic Sarcoma

Project description:This randomized phase I/II clinical trial is studying the side effects and best dose of gamma-secretase/notch signalling pathway inhibitor RO4929097 when given together with vismodegib and to see how well they work in treating patients with advanced or metastatic sarcoma. Vismodegib may slow the growth of tumor cells. Gamma-secretase/notch signalling pathway inhibitor RO4929097 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving vismodegib together with gamma-secretase/notch signalling pathway inhibitor RO4929097 may be an effective treatment for sarcoma.

| 2091475 | ecrin-mdr-crc

Changes in the chromatin accessibility landscape of mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Changes in the chromatin accessibility landscape of mouse embryonic endocardial cells after Notch pathway manipulation

| PRJNA927979 | ENA

Injury-activated endocardium plays structural and signalling roles in zebrafish heart regeneration

Project description:The zebrafish heart remarkably regenerates after a severe ventricular damage followed by inflammation, fibrotic tissue deposition and removal concomitant with cardiac muscle replacement. We have investigated the role of the endocardium in this regeneration process. 3D-whole mount imaging in injured hearts revealed that GFP-labelled endocardial cells in ET33mi-60A transgenic fish become rapidly activated and highly proliferative at 3 days post cryoinjury (dpci). Endocardial cells extensively expand within the injury site and organize to form a coherent structure at 9 dpci that persists throughout the regeneration process. Upon injury, endocardial cells strongly up-regulate the Notch pathway ligand delta like4 (dll4) and the Notch receptors notch1b, notch2 and notch3. Expression profiling showed that Notch signalling inhibition affects endocardial gene expression and genes related to extracellular matrix remodelling and inflammation. Gain- and loss-of-function experiments revealed that Notch is required for the organization of the endocardium, attenuation of the inflammatory response and cardiomyocyte proliferation. These results demonstrate a novel structural and signalling role for the endocardium during heart regeneration.

2017-03-31 | GSE68650 | GEO

Changes in gene expression in mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Analysis by RNA-seq of the changes in gene expression in MEEC due to the activity of Notch ligands.

2023-12-08 | GSE223734 | GEO

Changes in the chromatin accessibility landscape of mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Analysis by ATAC-seq of the changes in chromatin accessibility in MEEC due to the activity of Notch ligands.

2023-12-08 | GSE223733 | GEO

NOTCH signaling pathway is required for bovine early embryonic development

Project description:The NOTCH signaling pathway plays an important role in regulating various biological processes, including cell proliferation, lineage specification and apoptosis. Multiple components of the NOTCH pathway have been identified in mammalian preimplantation embryos. However, the precise role of NOTCH pathway in early embryonic development is poorly understood, especially in domestic animals. Here, we show that key transcripts of the NOTCH pathway exhibit a dynamic pattern throughout early embryonic development with an abundant level before embryonic genome activation in cattle. We also confirmed the presence of active NOTCH1 and RBPJ. By using pharmacological and RNAi tools, we demonstrated that the NOTCH pathway is required for the proper development of bovine early embryos. This functional consequence could be partly attributed to the major transcriptional mediator-RBPJ, whose deficiency also compromised the embryo quality. Indeed, we observed a significant increase of histone H3 serine 10 phosphorylation (pH3S10, a mitosis marker) positive blastomeres in not only NOTCH1 depleted embryos but RBPJ depleted ones. Importantly, RNA-seq analysis revealed that either NOTCH1 or RBPJ depletion triggers a reduction in H1FOO that encodes the oocyte-specific linker histone H1 variant. Interestingly, depleting H1FOO also results in detrimental effects on the developmental competence of early embryos, similar with NOTCH1 inhibition. Overall, our results reveal a crucial role for NOTCH pathway in regulating bovine preimplantation development, likely by controlling cell proliferation and maintaining H1FOO expression.

2021-01-31 | GSE158679 | GEO

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