Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257199 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1533754.fastq.gz | Fastqsanger.gz | |||
| SRR1533755.fastq.gz | Fastqsanger.gz | |||
| SRR1533756.fastq.gz | Fastqsanger.gz | |||
| SRR1533757.fastq.gz | Fastqsanger.gz | |||
| SRR1533758.fastq.gz | Fastqsanger.gz |
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Project description:Genome-wide DNA methylation analysis reveals dynamic changes in the cardiac methylome during post-natal heart development
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Project description:Genome-wide DNA methylation analysis reveals dynamic changes in the cardiac methylome during post-natal heart development (RNA-Seq)
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Project description:Epigenetic modifications have emerged as central players in the coordination of gene expression networks during cardiac development. While several studies have investigated the role of histone modifications during heart development, relatively little is known about the role of DNA methylation. The purpose of the current study was to determine whether DNA methylation plays an important role in guiding transcriptional changes during the neonatal period, which is an important developmental window for cardiac maturation and cardiomyocyte cell cycle arrest. We used methyl binding domain protein sequencing (MBD-seq) and mRNA-seq to profile DNA methyation and gene expression respectively in neonatal hearts at P1 and P14 stages. Thousands of differentially methylated regions (DMRs) were identified between P1 and P14, the vast majority of which were hypermethylated. Gene ontology analysis revealed that these hypermethylated genes were associated with transcriptional regulation of important developmental signaling pathways, including Hedgehog, BMP, TGF beta, FGF and Wnt/b-catenin signaling. A significant enrichment for myogenic transcription factors and Smad2/3/4 binding sites was also noted among differentially methylated peaks at P14. This study provides novel evidence for widespread alterations in DNA methylation during post-natal heart maturation and suggests that DNA methylation plays an important role in cardiomyocyte cell cycle arrest during the neonatal period. We used methyl binding domain protein sequencing (MBD-seq) to profile DNA methyation in neonatal hearts at P1 and P14 stages (post-natal day 1 and 14 respectively) in three biological replicates.
2014-08-01 | E-GEOD-59969 | biostudies-arrayexpress
Project description:Epigenetic modifications have emerged as central players in the coordination of gene expression networks during cardiac development. While several studies have investigated the role of histone modifications during heart development, relatively little is known about the role of DNA methylation. The purpose of the current study was to determine whether DNA methylation plays an important role in guiding transcriptional changes during the neonatal period, which is an important developmental window for cardiac maturation and cardiomyocyte cell cycle arrest. We used methyl binding domain protein sequencing (MBD-seq) and mRNA-seq to profile DNA methyation and gene expression respectively in neonatal hearts at P1 and P14 stages. Thousands of differentially methylated regions (DMRs) were identified between P1 and P14, the vast majority of which were hypermethylated. Gene ontology analysis revealed that these hypermethylated genes were associated with transcriptional regulation of important developmental signaling pathways, including Hedgehog, BMP, TGF beta, FGF and Wnt/b-catenin signaling. A significant enrichment for myogenic transcription factors and Smad2/3/4 binding sites was also noted among differentially methylated peaks at P14. This study provides novel evidence for widespread alterations in DNA methylation during post-natal heart maturation and suggests that DNA methylation plays an important role in cardiomyocyte cell cycle arrest during the neonatal period. mRNA-seq to profile gene expression in neonatal hearts at P1 and P14 stages (post-natal day 1 and 14 respectively) in three biological replicates.
2014-08-01 | E-GEOD-59970 | biostudies-arrayexpress
Project description:Epigenetic modifications have emerged as central players in the coordination of gene expression networks during cardiac development. While several studies have investigated the role of histone modifications during heart development, relatively little is known about the role of DNA methylation. The purpose of the current study was to determine whether DNA methylation plays an important role in guiding transcriptional changes during the neonatal period, which is an important developmental window for cardiac maturation and cardiomyocyte cell cycle arrest. We used methyl binding domain protein sequencing (MBD-seq) and mRNA-seq to profile DNA methyation and gene expression respectively in neonatal hearts at P1 and P14 stages. Thousands of differentially methylated regions (DMRs) were identified between P1 and P14, the vast majority of which were hypermethylated. Gene ontology analysis revealed that these hypermethylated genes were associated with transcriptional regulation of important developmental signaling pathways, including Hedgehog, BMP, TGF beta, FGF and Wnt/b-catenin signaling. A significant enrichment for myogenic transcription factors and Smad2/3/4 binding sites was also noted among differentially methylated peaks at P14. This study provides novel evidence for widespread alterations in DNA methylation during post-natal heart maturation and suggests that DNA methylation plays an important role in cardiomyocyte cell cycle arrest during the neonatal period.
2014-08-01 | GSE59970 | GEO
Project description:Epigenetic modifications have emerged as central players in the coordination of gene expression networks during cardiac development. While several studies have investigated the role of histone modifications during heart development, relatively little is known about the role of DNA methylation. The purpose of the current study was to determine whether DNA methylation plays an important role in guiding transcriptional changes during the neonatal period, which is an important developmental window for cardiac maturation and cardiomyocyte cell cycle arrest. We used methyl binding domain protein sequencing (MBD-seq) and mRNA-seq to profile DNA methyation and gene expression respectively in neonatal hearts at P1 and P14 stages. Thousands of differentially methylated regions (DMRs) were identified between P1 and P14, the vast majority of which were hypermethylated. Gene ontology analysis revealed that these hypermethylated genes were associated with transcriptional regulation of important developmental signaling pathways, including Hedgehog, BMP, TGF beta, FGF and Wnt/b-catenin signaling. A significant enrichment for myogenic transcription factors and Smad2/3/4 binding sites was also noted among differentially methylated peaks at P14. This study provides novel evidence for widespread alterations in DNA methylation during post-natal heart maturation and suggests that DNA methylation plays an important role in cardiomyocyte cell cycle arrest during the neonatal period.
2014-08-01 | GSE59969 | GEO
Project description:Cardiac fibrosis is a pathophysiologic hallmark of the aging heart. In the uninjured heart, cardiac fibroblasts exist in the quiescent state, but little is known about how proliferation rates and fibroblast transcriptional programs change throughout the lifespan of the organism from the immediate postnatal period to adult life and old age. Using EdU pulse labeling, we demonstrate that more than 50% of cardiac fibroblasts are actively proliferating in the first day of post-natal life. However, within 4 weeks of birth in the juvenile animal, only 10% of cardiac fibroblasts are proliferating. By early adulthood, the fraction of proliferating cardiac fibroblasts further decreases to approximately 2%, where it so remains throughout the rest of the organism’s life span. Examination of absolute cardiac fibroblast numbers demonstrated concordance with age related changes in fibroblast proliferation with no significant differences in absolute cardiac fibroblast numbers between animals 14 weeks and 1.5 years of age. We demonstrate that the maximal changes in cardiac fibroblast transcriptional programs and in particular collagen expression occur within the first weeks of life from the immediate postnatal to the juvenile period. We show that even though the aging heart exhibits an increase in the total amount of accumulated collagen, transcription of various collagens and ECM genes both in the heart and cardiac fibroblast is maximal in the newly born and juvenile animal and decreases with organismal aging. Examination of DNA methylation changes both in the heart and in cardiac fibroblasts did not demonstrate significant changes in differentially methylated regions between young and old mice. Our observations demonstrate that cardiac fibroblasts attain a stable proliferation rate and transcriptional program early in the life span of the organism and suggest a model of cardiac aging where phenotypic changes in the aging heart are not directly attributable to changes in proliferation rate or altered collagen expression in cardiac fibroblasts.
2020-10-26 | GSE160074 | GEO
Project description:The most common congenital heart disease (CHD) is the ventricular septal defect (VSD), which is also a subfeature of Tetralogy of Fallot (TOF) representing the most common form of cyanotic CHD. The underlying causes for the majority of CHDs are still unclear and most probably consist of combinations of genetic, epigenetic and environmental factors. DNA methylation is the most widely studied epigenetic modification and several cardiac regulators have already been shown to be differentially methylated in CHD patients. Here, we present the first analysis of genome-wide DNA methylation data obtained from cardiac biopsies of TOF and VSD patients. We applied affinity-based enrichment of methylated DNA sequences with methyl-CpG-binding domain proteins followed by next-generation sequencing (MBD-Seq). MBD-seq on cardiac biopsies of patients with Tetralogy of Fallot and ventricular septal defect
2016-08-08 | E-GEOD-62629 | biostudies-arrayexpress
Project description:In this study we evaluate the changes in m5C methylation at critical post-natal stages of brain development and links to methylation levels of neuronal stem cells and cortical neurons. We identify transcript-specific changes in methylation level associated with gene expression.
2022-08-11 | GSE207092 | GEO
Project description:Heart disease is the leading cause of death in the developed world, and its comorbidities such as hypertension, diabetes, and heart failure are accompanied by major transcriptomic changes in the heart. During cardiac dysfunction, which leads to heart failure, there are global epigenetic alterations to chromatin that occur concomitantly with morphological changes in the heart in response to acute and chronic stress. These epigenetic alterations include the reversible methylation of lysine residues on histone proteins. Lysine methylation on histone H3K4 and H3K9 were among the first methylated lysine residues identified and have been linked to gene activation and silencing, respectively. However, much less is known regarding other methylated histone residues, including histone H4K20. Trimethylation of histone H4K20 has been shown to repressive gene expression, however this mark has never been examined in the heart. Here we utilized immunoblotting and mass spectrometry to quantify histone H4K20 trimethylation in three models of cardiac dysfunction. Our results show that lysine methylation at this site is regulated in a biphasic manner leading to increased H420 trimethylation during acute hypertrophic stress and decreased H4K20 trimethylation during sustained ischemic injury and cardiac dysfunction. In addition, we examined publicly available datasets to analyze enzymes that regulate H4K20 methylation and identified one demethylase (KDM7C) and two methyltransferases (KMT5A and SMYD5) which were all upregulated in heart failure patients. This is the first study to examine histone H4K20 trimethylation in the heart and to determine how this post-translational modification is differentially regulated in multiple models of cardiac disease.
2022-10-14 | PXD031617 | Pride