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Differential gene expression in mouse skNAC knockout heart at E11.5

ABSTRACT: Targeted deletion of skNAC in mice resulted in early embryonic lethality with cardiac defects. In order to investigate the molecular mechanism of the cardiac defect, we designed the microarray comparing gene expression of the mutant E11.5 heart to wild type E11.5 heart. Keywords: genetic modification in mouse

ORGANISM(S): Mus musculus

PROVIDER: GSE5841 | GEO | 2010/11/19

SECONDARY ACCESSION(S): PRJNA97239

REPOSITORIES: GEO

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Differential gene expression in mouse skNAC knockout heart at E11.5

Project description:Targeted deletion of skNAC in mice resulted in early embryonic lethality with cardiac defects. In order to investigate the molecular mechanism of the cardiac defect, we designed the microarray comparing gene expression of the mutant E11.5 heart to wild type E11.5 heart. Keywords: genetic modification in mouse 3 for each genotypes, comparing Littermates of E11.5, total RNA (500ng) from ventricles, Affymetrix GeneChip Mouse Genome 430 2.0 Array

2010-11-19 | E-GEOD-5841 | biostudies-arrayexpress

Genome-wide analysis of epicardial gene expression in E11.5 mouse hearts

Project description:Identification of epicardium-enriched genes in the embryonic heart. The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in re-activation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. We established a mouse embryonic heart organ culture and gene expression system that facilitated the identification of epicardial enhancers activated during heart development and injury. Epicardial activation of these enhancers depends on a combinatorial transcriptional code centered on CCAAT/enhancer binding protein (C/EBP) transcription factors. Disruption of C/EBP signaling in the adult epicardium reduced injury-induced neutrophil infiltration and improved cardiac function. These findings reveal a transcriptional basis for epicardial activation and heart injury, providing a platform for enhancing cardiac regeneration. Total RNA obtained from lacZ-positive epicardial cells isolated from the E11.5 Tcf21lacZ hearts compared to total dissociated heart cells

2012-11-01 | E-GEOD-41959 | biostudies-arrayexpress

E11.5 Hand1 myocardial knockout RNA-Seq

Project description:Aims: To examine the role of the basic Helix-loop-Helix (bHLH) transcription factor HAND1 in embryonic and adult myocardium. Methods and Results: Hand1 is expressed within the cardiomyocytes of the left ventricle (LV) and myocardial cuff between embryonic days (E) 9.5-13.5. Hand gene dosage plays an important role in ventricular morphology and the contribution of Hand1 to congenital heart defects requires further interrogation. Conditional ablation of Hand1 was carried out using either Nkx2.5 knockin Cre (Nkx2.5Cre) or a-myosin heavy chain Cre (aMhc-Cre) driver. Interrogation of transcriptome data via Ingenuity Pathway Analysis (IPA) reveals several gene regulatory pathways disrupted including translation and cardiac hypertrophy-related pathways. Embryo and adult hearts were subjected to histological, functional and molecular analyses. Myocardial deletion of Hand1 results in morphological defects that include cardiac conduction system defects, survivable interventricular septal defects (VSDs), and abnormal LV papillary muscles (PM). Resulting Hand1 conditional mutants are born at Mendelian frequencies; but the morphological alterations acquired during cardiac development result in, the mice developing diastolic heart failure. Conclusions: Collectively, these data reveal that Hand1 contributes to the morphogenic patterning and maturation of cardiomyocytes during embryogenesis and although survivable, indicate a role for Hand1 conduction system and papillary morphogenesis.

2019-06-01 | GSE128571 | GEO

Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines (congenital heart disease)

Project description:Molecular Signatures of cardiac defects in Down syndrome lymphoblastoid cell lines. In this study, we want to identify genes and pathways specifically dysregulated in atrioventricular septal defect and /or atrial septal defect + ventricular septal defect in case of trisomy 21. Total RNA obtained from DS lymphoblastoid cell lines without congenital heart disease compared to cell lines from DS with congenital heart disease.

2012-08-14 | E-GEOD-34457 | biostudies-arrayexpress

Genome-wide maps of Nkx2-5 in E11.5 mouse embryonic heart

Project description:We report the identification of genome-wide binding site of the cardiac transcription factor Nkx2-5 during mouse heart development.

2015-09-02 | GSE44574 | GEO

Mesp1Cre;Hira-/fl and Mesp1Cre;Hira+/fl in heart at E11.5 and E12.5

Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from a Mesp1Cre driven ablation of Hira in the heart at E11.5 and E12.5. Methods: RNA extraction was done in triplicate from Mesp1Cre;Hira-/fl and Mesp1Cre;Hira+/fl embryonic hearts at E11.5 and E12.5 using the QIAGEN RNeasy mini kit. RNAseq was processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R package. Strand NGS 2.5 software was used to re-analyse the aligned files (.bam). By applying the Mann Whitney unpaired test, Benjamini Hochberg False discovery rate (FDR) and filtering the genes using adjusted p-value ≤ 0.05 and absolute fold change ≥ 1.5, 95 % of the results were identical to the DEseq package used by the UCL Genomics facility. Results: We identified 360 coding transcripts changed in the mutant hearts (Mann Whitney unpaired test, Benjamini Hochberg FDR, p ≤ 0.05, FC ≥ 1.5) with no trend towards up- or down-regulation of global transcription (48.8% down vs 51.2% up) at E12.5. Conclusions: This work analyses the role of HIRA in mouse cardiac development. It was found that Tnni2 is the most upregulated gene in the absence of Hira. qRT-PCR validation of 25 targets. Little (<5%) or no variation of fold change between RNAseq and qRT-PCR data were observed.

2016-08-12 | GSE79937 | GEO

Genome-wide maps of Nkx2-5 in E11.5 mouse embryonic heart

Project description:We report the identification of genome-wide binding site of the cardiac transcription factor Nkx2-5 during mouse heart development. Examination of Nkx2-5 binding in wild-type mouse in duplicate.

2015-09-02 | E-GEOD-44574 | biostudies-arrayexpress

RNA-seq of wild-type and Tbx20 homozygous knockout E11.5 mouse cardiomyocytes to study Tbx20's roles in embryonic and adult mouse heart function

Project description:Tbx20 is a transcription factor known to play important roles in embryonic and adult mouse heart function. Our goal in this work was to better understand the function of this gene in embryonic (E11.5) mouse cardiomyocytes that form the developing chambers, expanding our knowledge of its role in heart development. To elucidate the role of Tbx20 in mouse cardiomyocytes, we generated conditional Tbx20 knockout and compared 4 samples with 4 samples of wild-type cardiomyocytes. We found evidence of regulation of cell cycle genes by Tbx20, which are involved in proliferation. In addition, Tbx20 seems to bind and regulate an enhancer of CoupTFII in the atrium, a gene involved in atrial development.

2018-06-14 | E-MTAB-5596 | biostudies-arrayexpress

scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO)

Project description:We performed scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.

2022-07-27 | GSE198562 | GEO

scATAC-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO)

Project description:We performed scATAC-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.

2022-07-27 | GSE198561 | GEO

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