E-GEOD-51483
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA223290
PROVIDER: E-GEOD-51483 | ExpressionAtlas | 2015-07-27
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Transcriptional Atlas of Cardiogenesis Maps Congenital Heart Disease Interactome
| PRJNA223290 | ENA
Project description:Pathological cardiac hypertrophy is a leading cause of heart failure. The understanding of disease mechanisms is primarily based on experimental models, but knowledge of the full repertoire of cardiac cells and their gene expression profiles in the human heart is missing. Here, using large-scale single-nucleus transcriptomes, we highlight the transcriptional response of cardiomyocytes to pressure overload in humans with stenosis of the aortic valve and disclose major alterations in cellular cross-talk. Cardiomyocytes showed a reduction of incoming connections with endothelial cells and fibroblasts. Particularly Eph receptor tyrosine kinases, including the predominant EPHB1 gene, were significantly down-regulated in cardiomyocytes of the hypertrophied heart. We compared 5 AS patients to healthy patients from the human heart cell ATLAS (https://www.heartcellatlas.org). This repository contains the processed files from the single nuclei RNA-SEQ.
2021-12-06 | E-MTAB-11268 | biostudies-arrayexpress
Project description:Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, the transcriptional landscape of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide expression profile of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, prioritized stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling the bioinformatics of the congenital heart disease interactome, we deconstructed disease-centric regulatory networks encoded within this cardiogenic atlas to reveal stage-specific developmental disturbances clustered on epithelial-to-mesenchymal transition (EMT), BMP regulation, NF-AT signaling, TGFb-dependent induction, and Notch signaling. Therefore, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease. To interrogate the temporal and spatial expression profiles across the entire genome during mammalian heart development, we designed a time-course microarray experiment using the mouse model at defined stages of cardiogenesis, starting with embryonic stem cells (ESC, R1 stem cell line), early embryonic developmental stages: E7.5 whole embryos, E8.5 heart tubes, left and right ventricle tissues at E9.5, E12.5, E14.5, E18.5 to 3 days after birth (D3) and adult heart (Figure 1A). At each time point, microarray experiments were performed on triplicate biological samples. Starting at E9.5, tissue samples from left ventricles (LV) and right ventricles (RV) were microdissected for RNA purification and microarray analysis to determine spatially differential gene expression between LV and RV during heart development.
2014-05-19 | E-GEOD-51483 | biostudies-arrayexpress
Project description:Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, the transcriptional landscape of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide expression profile of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, prioritized stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling the bioinformatics of the congenital heart disease interactome, we deconstructed disease-centric regulatory networks encoded within this cardiogenic atlas to reveal stage-specific developmental disturbances clustered on epithelial-to-mesenchymal transition (EMT), BMP regulation, NF-AT signaling, TGFb-dependent induction, and Notch signaling. Therefore, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease.
2014-05-19 | GSE51483 | GEO
Project description:Epigenetic atlas of ageing mouse heart
2022-12-01 | E-MTAB-8826 | biostudies-arrayexpress
Project description:A Transcriptional Switch Governs Fibroblast Activation in Heart Disease
| PRJNA655922 | ENA
Project description:Cellular Atlas of Human Heart Failure
| PRJNA762100 | ENA
Project description:This study has two main goals. The first is to define a gene expression atlas of heart valve cells and identify cell heterogeneity within postnatal heart valve development. The second is to identify interstitial cell populations involved in ECM remodeling during postnatal heart valve development. Overall design: Using droplet RNA sequencing, transcriptomes of single cells from P7 and P30 murine aortic and mitral heart valves were analyzed.
2018-07-13 | E-HCAD-18 | biostudies-arrayexpress