Mechanistic basis of neonatal heart regeneration revealed by transcriptome and histone modification profiling
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA510088 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8318740.fastq.gz | Fastqsanger.gz | |||
| SRR8318750.fastq.gz | Fastqsanger.gz | |||
| SRR8318760.fastq.gz | Fastqsanger.gz | |||
| SRR8318800.fastq.gz | Fastqsanger.gz | |||
| SRR8318810.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 108 |
Similar Datasets
Project description:The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. To uncover the molecular mechanisms underlying neonatal heart regeneration, we compared the transcriptomes and epigenomes of regenerative and nonregenerative mouse hearts over a 7-d time period following myocardial infarction injury. By integrating gene expression profiles with histone marks associated with active or repressed chromatin, we identified transcriptional programs underlying neonatal heart regeneration, and the blockade to regeneration in later life. Our results reveal a unique immune response in regenerative hearts and a retained embryonic cardiogenic gene program that is active during neonatal heart regeneration. Among the unique immune factors and embryonic genes associated with cardiac regeneration, we identified Ccl24, which encodes a cytokine, and Igf2bp3, which encodes an RNA-binding protein, as previously unrecognized regulators of cardiomyocyte proliferation. Our data provide insights into the molecular basis of neonatal heart regeneration and identify genes that can be modulated to promote heart regeneration.
| S-EPMC6744882 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-07-15 | GSE123868 | GEO
Project description:Mechanistic basis for maintenance of CHG methylation in plants
| PRJNA749004 | ENA
Project description:Background: The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. To uncover the molecular mechanisms underlying neonatal heart regeneration, we compared the transcriptomes and epigenomes of regenerative and non-regenerative mouse hearts over a 7-day time period following myocardial infarction. Methods: RNA-Seq, H3K27ac ChIP-Seq and H3K27me3 ChIP-Seq were performed on ventricular samples from regenerative P1 or non-regenerative P8 mouse hearts at +1.5d, +3d and +7d after MI or Sham surgery to assemble the transcriptome, active chromatin and repressed chromatin landscapes during neonatal heart regeneration. Dynamic enhancer landscapes from mouse hearts during cardiac development were analyzed using data from ENCODE. Effects on cardiomyocyte proliferation and cardiac function from selected factors identified in this study were tested using BrdU/EdU pulse-labeling or mouse models coupled with immunohistochemistry and echocardiography. Results: By integrating gene expression profiles with histone marks associated with active or repressed chromatin, we identified transcriptional programs underlying neonatal heart regeneration and the blockade to regeneration in later life. Our results reveal a unique immune response in regenerative hearts and an embryonic cardiogenic gene program that remains active during neonatal heart regeneration. Among the unique immune factors and embryonic genes associated with cardiac regeneration, we identified Ccl24, which encodes a cytokine, and Igf2bp3, which encodes an RNA-binding protein, as previously unrecognized regulators of cardiomyocyte proliferation. Conclusions: Our data provide insights into the molecular basis of neonatal heart regeneration and identify genes that might be modulated to promote heart regeneration.
2019-07-15 | GSE123867 | GEO
Project description:Background: The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. To uncover the molecular mechanisms underlying neonatal heart regeneration, we compared the transcriptomes and epigenomes of regenerative and non-regenerative mouse hearts over a 7-day time period following myocardial infarction. Methods: RNA-Seq, H3K27ac ChIP-Seq and H3K27me3 ChIP-Seq were performed on ventricular samples from regenerative P1 or non-regenerative P8 mouse hearts at +1.5d, +3d and +7d after MI or Sham surgery to assemble the transcriptome, active chromatin and repressed chromatin landscapes during neonatal heart regeneration. Dynamic enhancer landscapes from mouse hearts during cardiac development were analyzed using data from ENCODE. Effects on cardiomyocyte proliferation and cardiac function from selected factors identified in this study were tested using BrdU/EdU pulse-labeling or mouse models coupled with immunohistochemistry and echocardiography. Results: By integrating gene expression profiles with histone marks associated with active or repressed chromatin, we identified transcriptional programs underlying neonatal heart regeneration and the blockade to regeneration in later life. Our results reveal a unique immune response in regenerative hearts and an embryonic cardiogenic gene program that remains active during neonatal heart regeneration. Among the unique immune factors and embryonic genes associated with cardiac regeneration, we identified Ccl24, which encodes a cytokine, and Igf2bp3, which encodes an RNA-binding protein, as previously unrecognized regulators of cardiomyocyte proliferation. Conclusions: Our data provide insights into the molecular basis of neonatal heart regeneration and identify genes that might be modulated to promote heart regeneration.
2019-07-15 | GSE123863 | GEO
Project description:The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. Neonatal heart regeneration is orchestrated by multiple cell types intrinsic to the heart, as well as immune cells that infiltrate the heart after injury. To elucidate the transcriptional responses of the different cellular components of the mouse heart following injury, we performed single cell RNA-sequencing on neonatal hearts at various time points following myocardial infarction, and coupled the results with bulk tissue RNA-sequencing data collected at the same time points. Concomitant single cell ATAC-sequencing exposed underlying dynamics of open chromatin landscapes and regenerative gene regulatory networks of diverse cardiac cell types, and revealed previously unknown mediators of cardiomyocyte proliferation, angiogenesis and fibroblast activation. Together, our data provide a transcriptional basis for neonatal heart regeneration at single cell resolution and suggest new strategies for enhancing cardiac function in response to injury.
2020-12-08 | GSE153480 | GEO
Project description:The adult mammalian heart has limited capacity for regeneration following injury, whereas the neonatal heart can readily regenerate within a short period after birth. Neonatal heart regeneration is orchestrated by multiple cell types intrinsic to the heart, as well as immune cells that infiltrate the heart after injury. To elucidate the transcriptional responses of the different cellular components of the mouse heart following injury, we performed single cell RNA-sequencing on neonatal hearts at various time points following myocardial infarction, and coupled the results with bulk tissue RNA-sequencing data collected at the same time points. Concomitant single cell ATAC-sequencing exposed underlying dynamics of open chromatin landscapes and regenerative gene regulatory networks of diverse cardiac cell types, and revealed previously unknown mediators of cardiomyocyte proliferation, angiogenesis and fibroblast activation. Together, our data provide a transcriptional basis for neonatal heart regeneration at single cell resolution and suggest new strategies for enhancing cardiac function in response to injury.
2020-12-08 | GSE153479 | GEO
Project description:Transcriptomic analysis of neonatal supporting cells after histone modification perturbations
| PRJNA630759 | ENA
Project description:The mechanistic basis of diverse, environmentally dependent genetic interaction in a metabolic pathway
| PRJNA475877 | ENA
Project description:Transcriptome profiling of neonatal heart regeneration
| PRJNA510091 | ENA