Effect of endothelial depletion of Wt1 on gene expression during coronary plexus sprouting in the heart
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA846722 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19572910.fastq.gz | Fastqsanger.gz | |||
| SRR19572911.fastq.gz | Fastqsanger.gz | |||
| SRR19572912.fastq.gz | Fastqsanger.gz | |||
| SRR19572913.fastq.gz | Fastqsanger.gz | |||
| SRR19572914.fastq.gz | Fastqsanger.gz |
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Project description:Coronary blood vessel formation is a highly regulated process in which endothelial cells (ECs) play an essential role. During the last years, new pieces of evidence have demonstrated WT1 expression in coronary ECs. However, its role in coronary blood vessel formation was almost unknown. Here we generated an inducible endothelial-specific Wt1KO mouse model (Wt1KOΔEC). The analysis of these mutant mice has demonstrated that deletion of Wt1 in coronary ECs impairs coronary blood vessels and myocardium development. The transcriptomic analysis of coronary ECs from Wt1KOΔEC mice demonstrated that deletion of Wt1 has a great impact on the molecular signature of coronary ECs that correlate with defects in cell proliferation, migration, and differentiation. These results provide novel insights into the role of WT1 in heart development and demonstrate that WT1 in ECs is required for coronary blood vessel formation.
2023-02-22 | GSE205616 | GEO
Project description:The elaborate patterning of coronary arteries critically supports the high metabolic activity of the beating heart. How coronary endothelial cells coordinate hierarchical vascular remodeling and achieve arteriovenous specification remains largely unknown. Understanding the molecular and cellular cues that pattern coronary arteries is crucial to develop innovative therapeutic strategies that restore functional perfusion within the ischemic heart. Single-cell transcriptomics were used to delineate heterogeneous transcriptional states of the developing and mature coronary endothelium with a focus on sprouting endothelium and arterial cell specification. We discovered that a tip-cell-to-artery specification mechanism drives arterialization of the intramyocardial plexus and endocardial tunnels throughout life. We also identified non-overlapping intramyocardial and subepicardial tip cell populations with differential gene expression profiles and regulatory pathways, suggesting that differential sprouting programs govern the formation and specification of the venous and arterial coronary plexus.
2024-07-25 | GSE223266 | GEO
Project description:Intramyocardial Sprouting Tip Cells Specify Coronary Arterialization
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Project description:Coronaries are essential for myocardial growth and heart function. Notch is crucial for mouse embryonic angiogenesis, but its role in coronary development remains uncertain. We show Jag1, Dll4 and activated Notch1 receptor expression in sinus venosus (SV) endocardium. Endocardial Jag1 removal blocks SV capillary sprouting, while Dll4 inactivation stimulates excessive capillary growth, suggesting that ligand antagonism regulates coronary primary plexus formation. Later endothelial ligand removal, or forced expression of Dll4 or the glycosyltransferase MFng, blocks coronary plexus remodeling, arterial differentiation, and perivascular cell maturation. Endocardial deletion of Efnb2 phenocopies the coronary arterial defects of Notch mutants. Angiogenic rescue experiments in ventricular explants, or in primary human endothelial cells, indicate that EphrinB2 is a critical effector of antagonistic Dll4 and Jag1 functions in arterial morphogenesis. Thus, coronary arterial precursors are specified in the SV prior to primary coronary plexus formation and subsequent arterial differentiation depends on a Dll4-Jag1-EphrinB2 signaling cascade.
2019-12-03 | GSE110614 | GEO
Project description:Atoh1-Cre; Myc/Myc mice developed choroid plexus papilloma and Atoh1-Cre; Myc/Myc; p53fl/fl mice developed choroid plexus carcinoma. By studying the gene expression profiles of normal choroid plexus, choroid plexus papilloma and choroid plexus carcinoma in mice, we aim to gain a better understanding of the biology of choroid plexus tumors
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Project description:This SuperSeries is composed of the following subset Series: GSE24440: Sprouting transcriptome in cortical neurons: young GSE24441: Sprouting transcriptome in cortical neurons: aged Refer to individual Series
2010-11-15 | E-GEOD-24442 | biostudies-arrayexpress
Project description:Several environmental pollutants have been reported to exhibit either pro-angiogenic or anti-angiogenic effects, which may contribute to related vascular diseases. However, the specific mechanism by which pollutants induce sprouting angiogenesis is unclear, and there are few studies on the association between the site of hyperangiogenesis and vascular diseases. In this study, zebrafish were exposed to bisphenol S (BPS, 1~100 µg/L) and tetrabromobisphenol S (TBBPS, 0.1 and 10 µg/L) from the embryonic to the larval stage to investigate how pollutants interfere with the function of ectopic sprouting vessels. Results showed that BPS and TBBPS promoted ectopic sprouting angiogenesis in different types of vascular plexus at different developmental time points but inhibited vascular endothelial-cadherin (VE-cadherin) expression. The proteomic analyses on eGFP-positive endothelial cells isolated from Tg(flk1: eGFP) zebrafish indicated that both BPS and TBBPS induced ectopic angiogenesis through inhibiting VE-cadherin-mediated adherens junction and activating the downstream pro-angiogenic signaling. In ectopic sprouting vessels induced by BPS and TBBPS, an increased endothelial permeability resulted in white blood cells recruitment and erythrocyte retention. Human oxidized lipids were also prone to deposit in these ectopic vessels following BPS and TBBPS exposure. This suggests that ectopic angiogenesis is a cause of vascular dysfunction and related diseases.
2024-11-12 | PXD057764 |
Project description:K-ras is one of the most frequently mutated human oncogenes. Activation of K-ras can lead to either senescence or proliferation in primary cells. The precise mechanism governing these distinct outcomes remains unclear. Here we utilized a loss-of-function screen to assess the role of specific genes identified as potential key regulators of K-ras driven oncogenesis. Using this approach, we identify the transcription factor Wt1 as an inhibitor of senescence in primary cells expressing oncogenic K-ras. Deletion or suppression of Wt1 expression leads to senescence of primary cells expressing oncogenic K-ras under the control of the native promotor at physiological levels, but has no effect on cells expressing wild-type K-ras. Wt1 contributes to K-ras driven lung tumorigenesis in vivo and loss of Wt1 is specifically deleterious to human lung cancer cell lines that are dependent on oncogenic K-ras. Taken together, these observations reveal a novel role for Wt1 as a key regulator of the complex genetic network required for the oncogenic effect of the small GTPase K-ras. We compare the expression profiles of Wild type, K-ras mutant, Wt1-null, and double K-ras mutant/Wt1-null mouse embryonic fibroblasts (MEFs). The study provides insights into the transcriptional role of Wt1 in the context of oncogenic K-ras.
2010-03-01 | GSE15325 | GEO
Project description:Interventions: A patient is vaccinated with Montanide ISA51-adjuvanted WT1 Trio cancer vaccine consisting of two WT1 CTL peptides (WT1-126 and WT1-235) and one WT1 HTL peptide (WT1-332) (2mg each) seven times at the interval of two weeks.
Primary outcome(s): Induction of WT1-specific immune responses assessed by WT1-related tests such as WT1-DTH skin reaction and serum levels of WT1 peptide IgG autoantibody at 1M, 2M, and 3M of WT1 Trio vaccine.
Study Design: Single arm Non-randomized
| 2638832 | ecrin-mdr-crc
Project description:Interventions: A patient is vaccinated with Montanide ISA51-adjuvanted WT1 Trio cancer vaccine consisting of two WT1 CTL peptides (WT1-126 and WT1-235) and one WT1 HTL peptide (WT1-332) (2mg each) seven times at the interval of two to four weeks. The interval can be changed within a range from one to 16 weeks.
Primary outcome(s): Induction of WT1-specific immune responses assessed by WT1-related tests such as WT1-DTH skin reaction, serum levels of WT1 peptide IgG autoantibody, and frequency of WT1-CTL in PB * This is evaluated at the interval ranging from 6 to 12 months.
Study Design: Single arm Non-randomized
| 2638831 | ecrin-mdr-crc