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Transcritptome analysis of anterior dorsal pericardial wall (aDPW) and cardiac outflow tract (OFT) from control and Hand2flox/flox; Mef2c-AHF-Cre embryos at E9.5

ABSTRACT: We aim to explore the gene expression difference in control and Hand2 mutant embryos and potential mechnisam downstream of Hand2 involved in OFT epithelium regulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE131362 | GEO | 2019/05/17

REPOSITORIES: GEO

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Transcritptome analysis of anterior dorsal pericardial wall (aDPW) and cardiac outflow tract (OFT) from control and Hand2flox/flox Mef2c-AHF-Cre embryos at E9.5

Project description:Transcritptome analysis of anterior dorsal pericardial wall (aDPW) and cardiac outflow tract (OFT) from control and Hand2flox/flox Mef2c-AHF-Cre embryos at E9.5

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Expression data from outflow region at E9.5

Project description:A high concentration of maternal retinoic acid (RA), the active derivative of vitamin A, is well known as a teratogenic agent which can cause developmental defects. Our previous studies have shown that the maternal administration of RA to mice within a narrow developmental window induces outflow tract (OFT) septum defects, which closely resembles human transposition of the great arteries (TGA), although the responsible factors and pathogenic mechanisms of the TGA induced by RA still remain unknown. To identify the candidate genes involved in the altered development of the OFT in RA-induce TGA model, we isolated the RNA from E9.5 control and RA-treated OFT regions, and performed a microarray analysis.

2011-11-08 | GSE33472 | GEO

Expression data from outflow region at E9.5

2011-11-08 | E-GEOD-33472 | biostudies-arrayexpress

Characterization of the effect of deleting the Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:To investigate the role of Gata6 in OFT development, we generated a Gata6 heterozygous mice, harvested OFT at E11.5, and determined gene expression profiles, using bulk RNA-seq.

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Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

2012-10-01 | GSE41179 | GEO

MEF2C regulates outflow tract alignment and transcriptional control of Tdgf1.

Project description:Congenital heart defects are the most common birth defects in humans, and those that affect the proper alignment of the outflow tracts and septation of the ventricles are a highly significant cause of morbidity and mortality in infants. A late differentiating population of cardiac progenitors, referred to as the anterior second heart field (AHF), gives rise to the outflow tract and the majority of the right ventricle and provides an embryological context for understanding cardiac outflow tract alignment and membranous ventricular septal defects. However, the transcriptional pathways controlling AHF development and their roles in congenital heart defects remain incompletely elucidated. Here, we inactivated the gene encoding the transcription factor MEF2C in the AHF in mice. Loss of Mef2c function in the AHF results in a spectrum of outflow tract alignment defects ranging from overriding aorta to double-outlet right ventricle and dextro-transposition of the great arteries. We identify Tdgf1, which encodes a Nodal co-receptor (also known as Cripto), as a direct transcriptional target of MEF2C in the outflow tract via an AHF-restricted Tdgf1 enhancer. Importantly, both the MEF2C and TDGF1 genes are associated with congenital heart defects in humans. Thus, these studies establish a direct transcriptional pathway between the core cardiac transcription factor MEF2C and the human congenital heart disease gene TDGF1. Moreover, we found a range of outflow tract alignment defects resulting from a single genetic lesion, supporting the idea that AHF-derived outflow tract alignment defects may constitute an embryological spectrum rather than distinct anomalies.

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Characterization of the effect of deleting the Mib1 and Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:To investigate the potential interactions between of Gata6 and Mib1 in OFT development, we generated a double heterozygous mice Mib1V943F/+ Gata6STOP/+, harvested OFT at E11.5, and determined gene expression profiles, using RNA-seq.

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Characterisation of the outflow tract banded heart utilising RNA sequencing to direct functional analysis

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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Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

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. Refer to individual Series

2010-05-17 | E-GEOD-17936 | biostudies-arrayexpress

Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

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.

2012-10-01 | E-GEOD-41179 | biostudies-arrayexpress

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