Single-cell sequencing of E10.5 mouse cardiac outflow tract
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE326956 | GEO | 2026/08/07
REPOSITORIES: GEO
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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. The outflow tract of control and ILK mutant mouse embryos at E10.5 were dissected and dissociated. Neural crest cells were FACS sorted and used for RNA extraction and hybridization on Affymetrix microarrays.
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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.
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Project description:The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression. This SuperSeries is composed of the SubSeries listed below.
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Project description:Gene expression profiling of the inferior and superior wall of the distal midgestation arterial domain (outflow tract) of the wild type CD1 mouse embryonic heart Total RNA was recovered from dissections of the inferior and superior OFT subdomains of Mus musculus littermate embryonic hearts at day 10.5 of development (E10.5). Dissections were performed in Rnase free DEPC treated cold PBS. Seven dissected samples of each domain were pooled for total RNA extraction with RNeasy kit according to the manufacturer’s instructions (Qiagen). For a quality control measure, total RNA was checked using the Agilent BioAnalyzer System (Agilent Technologies). RNA from each source was amplified and labeled with biotin. The labeled samples were hybridized to the Affymetrix GeneChip Mouse Genome 430 2.0
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Project description:Congenital heart disease (CHD) is a major birth defect affecting ~1% of new born babies. The OFT carries blood away from the heart into the great arteries. Defects specifically affecting the outflow tract (OFT) of the heart represent a third of all CHD cases. In humans the formation and remodelling of the OFT is a relatively rapid process, occurring over a 3-week period (Carnegie Stage (CS)13 – CS22). The morphological changes underlying OFT formation are orchestrated by two main cell lineages, second heart field (SHF)-derived myocardium and endothelium, and neural crest cells (NCC). Here, we present comprehensive transcriptomic data on the developing OFT at two distinct timepoint (embryonic and fetal) and its adult derivatives, providing a large reference framework of OFT cell repertoires and their gene expression profiles. This submission has the Adult dataset of this work.
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Project description:Congenital heart disease (CHD) is a major birth defect affecting ~1% of new born babies. The OFT carries blood away from the heart into the great arteries. Defects specifically affecting the outflow tract (OFT) of the heart represent a third of all CHD cases. In humans the formation and remodelling of the OFT is a relatively rapid process, occurring over a 3-week period (Carnegie Stage (CS)13 – CS22). The morphological changes underlying OFT formation are orchestrated by two main cell lineages, second heart field (SHF)-derived myocardium and endothelium, and neural crest cells (NCC). Here, we present comprehensive transcriptomic data on the developing OFT at two distinct timepoint (embryonic and fetal) and its adult derivatives, providing a large reference framework of OFT cell repertoires and their gene expression profiles. This submission has the Spatial Transcriptomics of this work.
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Project description:Heart development is known to be influenced by haemodynamics, however the effects of abnormal load on gene expression are not clearly defined. To determine the hearts transcriptional response to stress, a model of haemodynamic alteration, outflow tract (OFT) banding, was employed in the chick embryo at HH21. Stereological and expression analysis were performed at HH29, with targeted expression studies at HH35. We defined a phenotype of left sided heart dilation and performed RNA sequencing on OFT-banded hearts compared to Sham controls. Globin transcripts were depleted in the RNA during library preparation, and 28 differentially expressed genes were identified. Expression appeared to represent a mechanism of cardioprotection with calcium sequestering, metabolic and developmental genes highlighted. Significant reductions in apoptosis were also seen. We have presented a model of left sided dilation in OFT-banded hearts and found differential expression of genes that may be associated with stress and maintaining cardiac output.
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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. 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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