Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA325887 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The purpose of this study was to determine the effect of Nkx2.5 mutation (R141C) on gene expression in mouse embryonic stem cells during their differentiation into cardiac progenitors.
2017-12-31 | GSE83428 | GEO
Project description:Mouse embryonic stem cells can differentiate in vitro into spontaneously contracting cardiomyocytes. The main objective of this study was to investigate cardiogenesis in cultures of differentiating embryonic stem cells (ESCs) and to determine how closely it mimics in vivo cardiac development. We identified and isolated a population of cardiac progenitor cells (CPCs) through the use of a reporter DNA construct that allowed the expression of a selectable marker under the control of the Nkx2.5 enhancer. We proceeded to characterize these CPCs by examining their capacity to differentiate into cardiomyocytes and to proliferate. We then performed a large-scale temporal microarray expression analysis in order to identify genes that are uniquely upregulated or downregulated in the CPC population. We determined that the transcriptional profile of the mESC derived CPCs was consistent with pathways known to be active during embryonic cardiac development. We conclude that in vitro differentiation of mESCs recapitulates the early steps of mouse cardiac development. Keywords: embryonic stem cell, differentiation, cardiac progenitor, cardiogenesis
2007-08-30 | GSE5671 | GEO
Project description:We performed time-dependent, genome-wide analysis to explore gene expression profiles during in vitro cardiogenesis from embryonic stem cells to cardiac progenitor cells. Total RNA was extracted from undifferentiated stem cells, early mesodermal cells, cardiac mesodermal cells and cardiac progenitor cells. As a result of cluster analysis, Cited gene family was considered as candidate genes in cardiogenesis. Cited4 gene expression was specific for early cardiogenesis and Cited4 functioned as a cell cycle controling factor for early cardiac progenitor cells. Embryoid body was formed as in vitro cardiogenesis. Total RNA was extracted from Rex1-positive undifferentiated stem cells at day 0, Bra-positive early mesodermal cells at day 4.5, Flk1-positive cardiac mesodermal cells at day 4.5 and Nkx2.5-positive cardiac progenitor cells at day 7.5.
2016-03-31 | E-GEOD-63069 | biostudies-arrayexpress
Project description:The iTRAQ dataset for mouse embryonic stem cell differentiation.
2018-05-19 | MSV000082375 | MassIVE
Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis
2018-08-02 | MSV000082680 | GNPS
Project description:Cardiac differentiation of embryonic stem cells recapitulates embryonic cardiac development.
| PRJNA96951 | ENA
Project description:Metabolism is vital to cellular function and tissue homeostasis during human lung development. In utero, embryonic pluripotent stem cells undergo endodermal differentiation towards a lung progenitor cell fate that can be mimicked in vitro using induced human pluripotent stem cells (hiPSCs) to study genetic mutations. To identify differences between wild type and surfactant protein B (SFTPB)-deficient cell lines during endoderm specification towards lung, we used an untargeted metabolomics approach to evaluate the developmental changes in metabolites. We found that the metabolites most enriched during the differentiation from pluripotent stem cell to lung progenitor cell, regardless of cell line, were sphingomyelins and phosphatidylcholines, two important lipid classes in fetal lung development. The SFTPB mutation had no metabolic impact on early endodermal lung development. The identified metabolite signatures during lung progenitor cell differentiation may be utilized as biomarkers for normal embryonic lung development.
2021-06-29 | ST002055 | MetabolomicsWorkbench
Project description:The NK2 family of homeobox genes constitutes a family of transcription factors that play an important role in different developmental processes. Members of this group are characterized by two highly conserved protein domains: the homeodomain, conferring DNA binding activity, and the NK2-specific domain (NK2-SD) of yet unknown function. One of the best characterized members of this group is the early cardiogenic marker Nkx2.5. Loss of function of Nkx2.5 leads to embryonic lethality around E10.5 due to an arrest of heart development at the looping stage. We have further dissected the function of Nkx2.5 in vivo by creating a knockout mouse line harboring an in frame deletion of the NK2-SD by Cre/loxP mediated excision. Homozygous mutant mice die at E14.5 due to severe cardiac malformations, e.g. common AV canal, DORV, and VSD. Lack of the NK2-SD leads to downregulation of the ventricular markers MLC-2v and Irx4 specifically in the right ventricle, and is accompanied with reduced right ventricular function. This function of Nkx2.5 seems to be independent of its ability to bind target DNA, since lack of the NK2-SD does not alter the DNA binding activity of Csx/Nkx2.5 in vitro. Heterozygous mutant mice show a spectrum of cardiac defects related to cardiac septation and valve morphogenesis, but lack conduction system defects as reported for heterozygous Nkx2.5 mice. The phenotype observed in NK2-SD mutant mice shows that Nkx2.5 is not only crucial during early steps of cardiogenesis but also plays an important role at later developmental stages. Embryos were isolated at embryonic day 12.5. The entire embryo heart was taken and isolated in ice-cold PBS and immediately frozen on dry-ice. Total RNA was extracted from pooled samples of wildtype, heterozygous and mutant embryos.
2007-12-13 | E-GEOD-528 | biostudies-arrayexpress
Project description:Lack of the conserved NK2-domain of the cardiac transcription factor Nkx2.5 causes multiple heart defects . The NK2 family of homeobox genes constitutes a family of transcription factors that play an important role in different developmental processes. Members of this group are characterized by two highly conserved protein domains: the homeodomain, conferring DNA binding activity, and the NK2-specific domain (NK2-SD) of yet unknown function. One of the best characterized members of this group is the early cardiogenic marker Nkx2.5. Loss of function of Nkx2.5 leads to embryonic lethality around E10.5 due to an arrest of heart development at the looping stage. We have further dissected the function of Nkx2.5 in vivo by creating a knockout mouse line harboring an in frame deletion of the NK2-SD by Cre/loxP mediated excision. Homozygous mutant mice die at E14.5 due to severe cardiac malformations, e.g. common AV canal, DORV, and VSD. Lack of the NK2-SD leads to downregulation of the ventricular markers MLC-2v and Irx4 specifically in the right ventricle, and is accompanied with reduced right ventricular function. This function of Nkx2.5 seems to be independent of its ability to bind target DNA, since lack of the NK2-SD does not alter the DNA binding activity of Csx/Nkx2.5 in vitro. Heterozygous mutant mice show a spectrum of cardiac defects related to cardiac septation and valve morphogenesis, but lack conduction system defects as reported for heterozygous Nkx2.5 mice. The phenotype observed in NK2-SD mutant mice shows that Nkx2.5 is not only crucial during early steps of cardiogenesis but also plays an important role at later developmental stages. Embryos were isolated at embryonic day 12.5. The entire embryo heart was taken and isolated in ice-cold PBS and immediately frozen on dry-ice. Total RNA was extracted from pooled samples of wildtype, heterozygous and mutant embryos. Keywords = congenital heart disease, Csx, Nkx2.5 Keywords: other
2003-07-13 | GSE528 | GEO
Project description:DNA methylation mediated epigenetic regulation plays a critical role in regulating cardiomyocytes (CM) differentiation. Tet protein mediated DNA methylation oxidation have been reported to play an important role in regulating embryonic stem cell (ESC) differentiation toward different lineages. In our study, we utilized CRISPR/Cas9 based genome editing method to generated Tet single, double and triple deficient mouse ESC (mESC) expressing emGFP under NKX2.5 promoter and differentiated these cells toward CM progenitors. By modulating emGFP population as cardiac progenitor cells, we found that deletion of Tet1 and Tet2 significantly impairs mESC differentiation toward CM progenitors. Further single-cell RNA-seq analysis in differentiated control and Tet-triple knockout (TKO) mESC reveals that Tet deletion resulted in accumulation of mesoderm progenitors and impairs CM differentiation. Overexpression the catalytic domain of Tet1 could rescue the development defects in Tet-TKO mESC and restore NKX2.5 gene expression. In addition, loci-specific dCas9-Tet1CD mediated epigenome editing at Hand1 loci confirmed its directly transcriptional regulation during CM differentiation. Overall, out studies suggested that Tet protein mediated epigenomic remodeling is a genome-wide event and is essential to maintain proper transcription network during mESC differentiation toward CM progenitors.
2023-02-08 | GSE168061 | GEO