Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: yunfu sun
PROVIDER: E-GEOD-41179 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Neural crest defects lead to congenital heart disease involving outflow tract (OFT) malformation. Integrin-linked-Kinase (ILK) plays important roles in multiple cellular processes and embryogenesis. ILK is expressed in neural crest cells (NCC), but its role in NCC and OFT morphogenesis remains unknown. We used microarrays to detail the global programme of gene expression underlying the morphogenesis of the cardiac neural crest and outflow tract.
2012-10-01 | GSE41179 | GEO
Project description:Neural crest defects lead to congenital heart disease involving outflow tract (OFT) malformation. Integrin-linked-Kinase (ILK) plays important roles in multiple cellular processes and embryogenesis. ILK is expressed in neural crest cells (NCC), but its role in NCC and OFT morphogenesis remains unknown. We used microarrays to detail the global programme of gene expression underlying the morphogenesis of the cardiac neural crest and outflow tract.
2012-10-01 | GSE41179 | GEO
Project description:Cranial neural crest cells (NCC) give rise to the majority of the cartilage, bone, connective tissue, and sensory ganglia in the head, and also participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Our preliminary results show that targeted deletion of focal adhesion kinase (FAK) in murine NCC results in cardiovascular and craniofacial alterations, resembling human congenital heart diseases The objective of this project is to elucidate the underlying mechanisms by which FAK mediates NCC function during development. Compare gene expression in cranial neural crest cells of E11.5 wild type and FAK mutants. FAK is a tyrosine kinase that transduces integrin and growth factor signaling pathways. Abnormal growth factor signaling leads to cardiovascular malformations caused by deficient cardiac NCC function. However, a direct role for FAK in NCC morphogenesis has not been demonstrated. We will test the hypothesis that FAK is a downstream target of essential growth factor signaling in cranial neural crest cells during development. 1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis.
2008-06-11 | E-GEOD-11149 | biostudies-arrayexpress
Project description:Retinoic acid (RA), the bioactive derivative of vitamin A, is essential for vertebrate heart development. Both excess and reduced RA signaling lead to cardiovascular malformations, particularly affecting the cardiac outflow tract (OFT). The cellular mechanisms underlying the effects of RA signaling during OFT morphogenesis are not fully understood. To address this question, we used transient maternal RA supplementation to rescue the early lethality resulting from inactivation of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene. By embryonic day 13.5, Raldh2-/- hearts exhibited OFT septation defects. Although cardiac neural crest cells (cNCC) were present in OFT cushions of Raldh2-/- mutant embryos, we observed that cNCC were ectopically located in the peripheral region of the endocardial cushions, closer to the myocardium rather than immediately subjacent to the endocardium. Mislocated cNCC were aligned in parallel instead of perpendicular arrays to the endocardial surface within the proximal OFT. Supernumerary mesenchyme was generated both in and ex vivo within the cushions by Raldh2-/- mutant endocardium and found in place of the cNCC in a subendocardial, medial position. Although mislocated and misoriented, mutant cNCC resembled wildtype cells in their compaction density and individually elongated shape. Our data show that RA signaling acts on cNCC orientation relative to the septation plane and position within OFT cushions during septation process. Transcriptomic analysis and pathway-specific readout suggest that up-regulation of the Bmp pathway may be responsible for increased endothelial-to-mesenchymal transition, leading thereby to displacement of cNCC. E10.5 stage embryonic mouse outflow tracts were microdissected. Four pools of four outflow tracts were established for wildtype (WT) and mutant (Raldh2-/-) embryos derived from dams whose food had been supplemented with all-trans-RA (Sigma) directly mixed into powdered food at 0.1 mg/g food and offered between E7.5 and E8.5. Total RNA was extracted using Macherey-Nagel NucleoSpin® RNA columns without on-column DNase digestion.
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Project description:Cranial neural crest cells (NCC) give rise to the majority of the cartilage, bone, connective tissue, and sensory ganglia in the head, and also participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardiovascular development. Our preliminary results show that targeted deletion of focal adhesion kinase (FAK) in murine NCC results in cardiovascular and craniofacial alterations, resembling human congenital heart diseases The objective of this project is to elucidate the underlying mechanisms by which FAK mediates NCC function during development. Compare gene expression in cranial neural crest cells of E11.5 wild type and FAK mutants. FAK is a tyrosine kinase that transduces integrin and growth factor signaling pathways. Abnormal growth factor signaling leads to cardiovascular malformations caused by deficient cardiac NCC function. However, a direct role for FAK in NCC morphogenesis has not been demonstrated. We will test the hypothesis that FAK is a downstream target of essential growth factor signaling in cranial neural crest cells during development. 1) Generate E11.5 mouse embryos that are either control (FAK+/flox) or NCC specific FAK knockout (Wnt1Cre;FAKflox/flox). 2) Determine genotype by PCR. 3) Dissect head and torax from the different genotypes. 4) Obtain NCC from dissected tissue by magnetic cell sorting using p75 antibody. 5) Prepare total RNA from speciments. We will pool the NCC from 3 different embryos of the same genotype, and send total RNA to TGEN for probe preparation, hybridization and array result analysis. Keywords: other
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Project description:S23 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E11.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E11.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 220 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E10.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 221 experiment: Our research has shown that heterozygous deletion of the miRNA processing enzyme Dicer leads to developmental delay of the thymus in mouse embryos. We sought to identify the microRNAs (miRNAs) affected by the loss of a single copy of Dicer in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring a floxed allele of Dicer, Cre-recombinase under the control of the Wnt1 NCC-specific promoter, and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) cells from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos via FACS and compared the relative expression of miRNAs in the Dicer-heterozygotes compared to Dicer-wildtypes by miRNA microarray. S23 experiment: RNA from YFP+ (NCCs) and YFP- (non-NCCs) cells sorted by FACS from E11.5 Wnt1Cre-R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from five E11.5 embryos were sorted into YFP+ and YFP- populations and pooled. 220 experiment: RNA from YFP+ (NCCs) and YFP- (non-NCCs) cells sorted by FACS from E10.5 Wnt1Cre-R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from ten E10.5 embryos were sorted into YFP+ and YFP- populations and pooled. 221 experiment: RNA from YFP+ (NCCs) cells sorted by FACS from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from ten embryos were sorted into YFP+ populations and pooled for each genotype.
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Project description:Retinoic acid (RA), the bioactive derivative of vitamin A, is essential for vertebrate heart development. Both excess and reduced RA signaling lead to cardiovascular malformations, particularly affecting the cardiac outflow tract (OFT). The cellular mechanisms underlying the effects of RA signaling during OFT morphogenesis are not fully understood. To address this question, we used transient maternal RA supplementation to rescue the early lethality resulting from inactivation of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene. By embryonic day 13.5, Raldh2-/- hearts exhibited OFT septation defects. Although cardiac neural crest cells (cNCC) were present in OFT cushions of Raldh2-/- mutant embryos, we observed that cNCC were ectopically located in the peripheral region of the endocardial cushions, closer to the myocardium rather than immediately subjacent to the endocardium. Mislocated cNCC were aligned in parallel instead of perpendicular arrays to the endocardial surface within the proximal OFT. Supernumerary mesenchyme was generated both in and ex vivo within the cushions by Raldh2-/- mutant endocardium and found in place of the cNCC in a subendocardial, medial position. Although mislocated and misoriented, mutant cNCC resembled wildtype cells in their compaction density and individually elongated shape. Our data show that RA signaling acts on cNCC orientation relative to the septation plane and position within OFT cushions during septation process. Transcriptomic analysis and pathway-specific readout suggest that up-regulation of the Bmp pathway may be responsible for increased endothelial-to-mesenchymal transition, leading thereby to displacement of cNCC.
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