Activation of NOTCH and BMP signaling pathways during acute hypoxic stress in cardiac mesenchymal cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA833422 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18972630.fastq.gz | Fastqsanger.gz | |||
| SRR18972631.fastq.gz | Fastqsanger.gz | |||
| SRR18972632.fastq.gz | Fastqsanger.gz | |||
| SRR18972633.fastq.gz | Fastqsanger.gz | |||
| SRR18972634.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:To analyze early transcriptional events in cardiac tissue after infarction and evaluate the genetic expression profile of post-infarction mesenchymal cells of the heart, we induced myocardial infarction in rats by ligation of the left coronary artery. 24 hours after surgery, the affected area was harvested for RNA isolation and cell culture. We then performed a gene expression profile analysis using data obtained from RNA sequencing of 3 different postinfarction tissues and cells. Healthy tissues and cells of the left ventricle of the heart of sham-operated rats were used as controls.
2022-05-02 | GSE201888 | GEO
Project description:Cardiac mesenchymal stem cells (C-MSC) are a novel mesenchymal stem cell subpopulation derived from cardiac tissue, whichi are reported to be responsible for cardiac regeneration. Notch siganling is believed to aid in cardiac repair following myocardial injury.Here, we investigated the difference of protein cargo content among extracellular vesicles from wild type C-MSC, Notch1 knock out C-MSC and Notch1 activated C-MSC.
2020-05-27 | PXD016578 | Pride
Project description:The aim of this study was to identify genes that are regulated by Bmp signaling with the zebrafish heart at the heart cone stage around 21-23 hours post fertilization. In total, 4 samples based on cDNA from extracted cardiac tissue were analyzed: 2 samples of Tg(hsp70l:bmp2b)fr13 transgenic embryos heatshocked at 18 hpf and 2 WT control samples.
2013-03-25 | E-GEOD-43888 | biostudies-arrayexpress
Project description:Progenitor cells of the first and second heart fields (FHF and SHF) depend on cardiac-specific transcription factors for their differentiation. In mouse mutant embryos, we define the hierarchy of signaling events that controls the expression of cardiac-specific transcription factors during commitment of SHF progenitors at E9.25. Wnt and Bmp act downstream of Notch/RBPJ at this developmental stage. Mutation of Axin2, the negative regulator of canonical Wnt signaling, enhances Wnt and Bmp signals and suffices to rescue the cardiac differentiation arrest caused by loss of RBPJ. By analysis of isolated cardiac progenitors, embryo cultures in the presence of pharmacological inhibitors, and Bmp triple mutants, we could classify the expression of heart-specific transcription factors of SHF progenitors according to their dependence on either Wnt or Bmp signals, Nkx2-5, Isl1, Baf60c and Gata4, SRF, Mef2c, respectively. Total RNA from whole embryonic hearts of control mice was compared to MesP1-cre:RBPJlox/lox (KO), MesP1-cre:RBPJlox/lox//Axin2-/- (DKO), MesP1-cre:RBPJlox/+//Axin2-/- (hetDKO) and MesP1-cre:RBPJlox/lox//Axin2+/- (DKOhet) mutant mouse embryos.
2012-06-20 | E-GEOD-36804 | biostudies-arrayexpress
Project description:During early development multiple progenitor populations contribute to the formation of the four-chambered heart and its diverse lineages. However, the underlying mechanisms that result in the specification of these progenitor populations are not yet fully understood. We have recently identified a population of cells that gives rise selectively to cardiovascular cells of the heart ventricles. Here, we have used this knowledge to isolate and profile subsets of cardiac mesoderm cells from the mouse embryo and have identified an enrichment for the Notch signaling pathway in ventricular cardiac mesoderm. Using the pluripotent stem cell differentiation system to investigate the role of Notch in a temporally controlled manner, we show that Notch induction increases cardiomyocyte differentiation efficiency. This is due to the enhanced specification of mesoderm to the cardiac lineage. Finally, our data suggests that Notch interacts with WNT signaling to enhance commitment to the cardiac lineage. Overall, our findings support the notion that key signaling events during early heart development are critical for proper lineage specification and segregation and provide additional detail into these processes in mouse and human cardiogenesis.
2023-01-07 | GSE143227 | GEO
Project description:During early development multiple progenitor populations contribute to the formation of the four-chambered heart and its diverse lineages. However, the underlying mechanisms that result in the specification of these progenitor populations are not yet fully understood. We have recently identified a population of cells that gives rise selectively to cardiovascular cells of the heart ventricles. Here, we have used this knowledge to isolate and profile subsets of cardiac mesoderm cells from the mouse embryo and have identified an enrichment for the Notch signaling pathway in ventricular cardiac mesoderm. Using the pluripotent stem cell differentiation system to investigate the role of Notch in a temporally controlled manner, we show that Notch induction increases cardiomyocyte differentiation efficiency. This is due to the enhanced specification of mesoderm to the cardiac lineage. Finally, our data suggests that Notch interacts with WNT signaling to enhance commitment to the cardiac lineage. Overall, our findings support the notion that key signaling events during early heart development are critical for proper lineage specification and segregation and provide additional detail into these processes in mouse and human cardiogenesis.
2023-01-07 | GSE143226 | GEO
Project description:Progenitor cells of the first and second heart fields (FHF and SHF) depend on cardiac-specific transcription factors for their differentiation. In mouse mutant embryos, we define the hierarchy of signaling events that controls the expression of cardiac-specific transcription factors during commitment of SHF progenitors at E9.25. Wnt and Bmp act downstream of Notch/RBPJ at this developmental stage. Mutation of Axin2, the negative regulator of canonical Wnt signaling, enhances Wnt and Bmp signals and suffices to rescue the cardiac differentiation arrest caused by loss of RBPJ. By analysis of isolated cardiac progenitors, embryo cultures in the presence of pharmacological inhibitors, and Bmp triple mutants, we could classify the expression of heart-specific transcription factors of SHF progenitors according to their dependence on either Wnt or Bmp signals, Nkx2-5, Isl1, Baf60c and Gata4, SRF, Mef2c, respectively.
2012-06-21 | GSE36804 | GEO
Project description:Beclin1 plays significant roles in cardiac organogenesis. Beclin1 can regulate the fate conversion of fibroblasts into cardiomyocytes. However, the function and mechanism of Beclin1 in regulating early cardiac lineage commitment and differentiation remain unclear. To explore its potential role in cardiac lineage development, we utilized model of cardiomyocyte differentiation from mouse embryonic stem cells (mESCs) to simulate early cardiogenesis and investigated the function of Beclin1. We show that the knockdown of Beclin1 facilitates cardiomyocyte differentiation. Through bulk RNA-sequencing analysis, we found that knocking down Beclin1 activated the Wnt signaling pathway at the embryoid body stage but inhibited its activity at the cardiomyocyte stage. Moreover, the Bone morphogenetic protein (Bmp) signaling pathway was continuously activated throughout cardiomyocyte differentiation process. Our findings demonstrate a novel function of Beclin1 during cardiac differentiation. The activation of Wnt-mediated Bmp signaling pathway represents a major mechanism by which the deficiency of Beclin1 promotes mESCs differentiation into cardiomyocytes.
2025-12-04 | GSE293719 | GEO
Project description:Hyperactivation of Notch signaling and the cellular hypoxic response are frequently observed in cancers, with increasing reports of connections to tumor initiation and progression. The two signaling mechanisms are known to intersect, but while it is well established that hypoxia regulates Notch signaling, less is known about whether Notch can regulate the cellular hypoxic response. We now report that Notch signaling specifically controls expression of HIF2a, a key mediator of the cellular hypoxic response. Transcriptional upregulation of HIF2a by Notch under normoxic conditions leads to elevated HIF2a protein levels in primary breast cancer cells as well as in human breast cancer, medulloblastoma and renal cell carcinoma cell lines. The elevated level of HIF2a protein was in certain tumor cell types accompanied by down-regulation of HIF1a protein levels, indicating that high Notch signaling may drive a HIF1a-to-HIF2a switch. At the transcriptome level, the presence of HIF2a was required for approximately 21% of all Notch-induced genes: among the 1062 genes that were upregulated by Notch in medulloblastoma cells during normoxia, upregulation was abrogated in 227 genes when HIF2a expression was knocked down by HIF2a siRNA. In conclusion, our data show that Notch signaling affects the hypoxic response via regulation of HIF2a, which may be important for future cancer therapies.
2018-04-19 | GSE113353 | GEO
Project description:Notch Activation Commits Mesoderm Cells to the Cardiac Lineage
| PRJNA599354 | ENA