Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA217955 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR964790_1.fastq.gz | Fastqsanger.gz | |||
| SRR964790_2.fastq.gz | Fastqsanger.gz | |||
| SRR964791_1.fastq.gz | Fastqsanger.gz | |||
| SRR964791_2.fastq.gz | Fastqsanger.gz | |||
| SRR964792_1.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptome modulation of ventricles, cardiomyocytes and cardiac fibroblasts during postnatal mouse development
2016-09-23 | E-GEOD-49906 | ExpressionAtlas
Project description:During development the fetal heart undergoes a rapid and dramatic transition to adult function through transcriptional and post-transcriptional mechanisms, including alternative splicing (AS). We performed deep RNA-sequencing for high-resolution analysis of transcriptome changes during postnatal mouse heart development using RNA from ventricles and freshly isolated cardiomyocytes (CM) and cardiac fibroblasts (CF). Extensive changes in gene expression and AS occur primarily between postnatal days 1 and 28. CM and CF showed reciprocal regulation of gene expression during postnatal development reflecting differences in proliferative capacity, cell adhesion functions, and mitochondrial metabolism. We found that AS plays a novel role in vesicular trafficking and membrane organization during postnatal CM development. Interestingly, these AS transitions are enriched among targets of two RNA-binding proteins, Celf1 and Mbnl1, which undergo developmentally regulated change in expression. Vesicular traffic genes affected by AS during normal development where Celf1 is down-regulated, showed a reversion to neonatal AS patterns when Celf1 was over-expressed in adults. RNA-seq was performed in RNA samples of ventricles, cardiomyocytes or cardiac fibroblast at different developmental stages; embryonic day 17, postnatal day (PN) 1, 10, 28 and 90 for ventricles, PN1-3, PN28 and PN60 for cardiac fibroblasts, and PN1-2, PN30, and PN67 for cardiomyocytes
2014-04-16 | E-GEOD-49906 | biostudies-arrayexpress
Project description:During development the fetal heart undergoes a rapid and dramatic transition to adult function through transcriptional and post-transcriptional mechanisms, including alternative splicing (AS). We performed deep RNA-sequencing for high-resolution analysis of transcriptome changes during postnatal mouse heart development using RNA from ventricles and freshly isolated cardiomyocytes (CM) and cardiac fibroblasts (CF). Extensive changes in gene expression and AS occur primarily between postnatal days 1 and 28. CM and CF showed reciprocal regulation of gene expression during postnatal development reflecting differences in proliferative capacity, cell adhesion functions, and mitochondrial metabolism. We found that AS plays a novel role in vesicular trafficking and membrane organization during postnatal CM development. Interestingly, these AS transitions are enriched among targets of two RNA-binding proteins, Celf1 and Mbnl1, which undergo developmentally regulated change in expression. Vesicular traffic genes affected by AS during normal development where Celf1 is down-regulated, showed a reversion to neonatal AS patterns when Celf1 was over-expressed in adults.
2014-04-16 | GSE49906 | GEO
Project description:Cardiac maturation lays the foundation for postnatal heart development and disease, yet little is known about the contributions of the microenvironment to cardiomyocyte maturation. By integrating single-cell RNA-sequencing data of mouse hearts at multiple postnatal stages, we construct cellular interactomes and regulatory signaling networks. Here we report switching of fibroblast subtypes from a neonatal to adult state and this drives cardiomyocyte maturation. Molecular and functional maturation of neonatal mouse cardiomyocytes and human embryonic stem cell-derived cardiomyocytes are considerably enhanced upon coculture with corresponding adult cardiac fibroblasts. Further, single-cell analysis of in vivo and in vitro cardiomyocyte maturation trajectories identify highly conserved signaling pathways, pharmacological targeting of which substantially delays cardiomyocyte maturation in postnatal hearts, and markedly enhances cardiomyocyte proliferation and improves cardiac function in infarcted hearts. Together, we identify cardiac fibroblasts as a key constituent in the microenvironment promoting cardiomyocyte maturation, providing insights into how the manipulation of cardiomyocyte maturity may impact on disease development and regeneration.
2020-04-20 | GSE122706 | GEO
Project description:Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation. To identify candidate fibroblast-derived factors that promote myocyte proliferation, we isolated RNA from Nkx-YFP+ cardiomyocytes, embryonic cardiac fibroblasts, and adult cardiac fibroblasts and profiled mRNA expressions by microarray analyses. Arrays were performed using Affymetrix mouse Gene 1.0 ST arrays. Analysis was performed on three biological replicates of mouse embyonic cardiomyocytes, fibroblasts and adult cardiac fibroblasts.
2009-01-14 | E-GEOD-14412 | biostudies-arrayexpress
Project description:Gene expression in mouse embyonic cardiomyocytes, fibroblasts and adult cardiac fibroblasts
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Project description:During the first weeks after birth, cardiomyocytes within the mouse heart progressively exit the cell cycle, binucleate, and lose regenerative capacity. We have determined that combined pharmacological inhibition of thyroid hormone and adrenergic signaling during postnatal development robustly enhances cardiomyocyte proliferation, retention of diploid cardiomyocytes, and functional cardiac regeneration at postnatal day 14. In this study, we perform transcriptome-wide analyses to understand the genetic pathways regulated by thyroid hormone, alpha-adreneric, and beta-adrenergic signaling - individually and in combination - that promote cardiomyocyte cell-cycle arrest and loss of cardiac regenerative potential.
2021-09-22 | GSE174511 | GEO
Project description:Growth and expansion of ventricular chambers is essential during cardiogenesis and is achieved by proliferation of cardiac progenitors that are not fully differentiated. Disruption of this process can lead to prenatal lethality. In contrast, adult cardiomyocytes achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Moreover, the function of embryonic cardiac fibroblasts, derived from epicardium, and their secreted factors are largely unknown. Using a novel co-culture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. b1 integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of b1 integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation. This SuperSeries is composed of the following subset Series: GSE14411: Gene expression in b1-integrin wild-type and knockout mouse heart GSE14412: Gene expression in mouse embyonic cardiomyocytes, fibroblasts and adult cardiac fibroblasts Refer to individual Series
2009-01-14 | E-GEOD-14414 | biostudies-arrayexpress
Project description:Cardiomyocytes and cardiac fibroblasts undergo coordinated maturation after birth, and cardiac fibroblasts are required for postnatal cardiomyocyte maturation in mice. Here, we investigate the role of cardiac fibroblast-expressed Growth Differentiating Factor 10 (GDF10) in postnatal heart development. In neonatal mice, Gdf10 is expressed specifically in cardiac fibroblasts, with its highest expression coincident with onset of cardiomyocytes cell cycle arrest and transition to hypertrophic growth. In neonatal rat ventricular myocyte cultures, GDF10 treatment promotes cardiomyocyte maturation indicated by increased binucleation, downregulation of cell cycle progression genes and upregulation of cell cycle inhibitor genes. GDF10 treatment leads to an increase in cardiomyocyte cell size together with increased expression of mature sarcomeric protein isoforms and decreased expression of fetal cardiac genes. RNAsequencing of GDF10-treated NRVM shows an increase in gene expression related to myocardial maturation, including upregulation of sodium and potassium channel genes. In vivo, loss of Gdf10 leads to a delay in myocardial maturation indicated by a decrease in cardiomyocyte cell size and binucleation as well as increased mitotic activity at postnatal (P) day 7. Further, induction of mature sarcomeric protein isoform gene expression is delayed, and expression of cell cycle progression genes is prolonged. However, by P10 indicators of cardiomyocyte maturation and mitotic activity are normalized in Gdf10-null hearts relative to controls. Together, these results implicate Gdf10 as a novel crosstalk mediator between cardiomyocytes and cardiac fibroblasts, required for appropriate timing of cardiomyocyte maturation steps including binucleation, hypertrophy, mature sarcomeric isoform switch and cell cycle arrest in the postnatal period.
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Project description:The significance of cardiac stem cell (CSC) populations for cardiac regeneration remains disputed. Here, we apply the most direct definition of stem cell function (the ability to replace lost tissue through cell division) to interrogate the existence of CSCs. By single-cell mRNA sequencing and genetic lineage tracing using two Ki67 knockin mouse models, we map all proliferating cells and their progeny in homoeostatic and regenerating murine hearts. Cycling cardiomyocytes were only robustly observed in the early postnatal growth phase, while cycling cells in homoeostatic and damaged adult myocardium represented various noncardiomyocyte cell types. Proliferative postdamage fibroblasts expressing follistatin-like protein 1 (FSTL1) closely resemble neonatal cardiac fibroblasts and form the fibrotic scar. Genetic deletion of Fstl1 in cardiac fibroblasts results in postdamage cardiac rupture. We find no evidence for the existence of a quiescent CSC population, for transdifferentiation of other cell types toward cardiomyocytes, or for proliferation of significant numbers of cardiomyocytes in response to cardiac injury.
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