The transcriptome and methylome of neonatal murine hearts
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PROVIDER: PRJNA282967 | ENA |
REPOSITORIES: ENA
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Project description:Neonatal murine cardiomyocyte transcriptome
| PRJNA795099 | ENA
Project description:The neonatal murine heart is able to regenerate after severe injury, however this capacity quickly diminishes within the first week of life. Since DNA methylation is one of epigenetic mechanisms that plays a crucial role in cell development and gene expression regulation, we explored the changes of DNA methylation and gene expression patterns which accompany the loss of the transient regenerative potential in the heart. We used MeDIP-chip approach in order to compare global DNA methylation profiles in the murine hearts at 1 day and 7 days after birth, as well as, in hearts of mice at the age of 2 and 8 weeks. The comparison exposed a number of DNA promoter regions significantly changing their DNA methylation status between these time-points. As the result a number of DMRs have been identified which show an overrepresentation of genes which are critical for proper heart maturation and muscle development. The methylome transition from d1 to d7 is characterized by the excess of gene regulatory regions which gain over those that lose DNA methylation, thus suggesting that a number of genes active at d1 are repressed at d7.
2016-12-31 | GSE68523 | GEO
Project description:The heart of a newborn mouse has an exceptional capacity to regenerate from myocardial injury but lose it after a week of life, which has been utilized as a valuable model to explore the cues for heart regeneration. More and more researches indicated that glycoprotein played an important role in cardiac regeneration. Elucidating the glycosylation processes associated with heart regeneration will be beneficial for the molecular mechanism studies of heart regeneration as well as discovery of potential therapeutic strategies for human cardiac diseases. In this work, an integrated glycoproteomic and proteomic analysis were performed to investigate the differences in glycoprotein abundances and site-specific glycosylation occupancy between neonatal day 1 (P1) and day 7 (P7) of mouse hearts. The intact glycoepeptides were enriched and identified in both P1 and P7 hearts. To screen for differentially regulated glycoproteins, we compared the expression levels of intact glycopeptides between P1 and P7 hearts using label free quantification. Eventually, the glycosylation occupancy of site-specific N-glycans were obtained by comparing the alterations of intact glycopeptides with their corresponding protein expression levels obtained from global proteomic analysis. These altered glycosylation patterns among proteins between P1 and P7 mouse hearts have a significant potential to aid our understanding of the regenerative capacity loss in neonatal mouse hearts during the first week, thus leading to novel therapeutic approaches to recover the capacity.
2020-05-26 | PXD017139 | Pride
Project description:Whole transcriptome analysis of neonatal mice hearts after myocardial infarction
| PRJNA814526 | ENA
Project description:m5C methylome, transcriptome and proteome of sysnechocystis
2024-08-29 | PXD055431 |
Project description:This SuperSeries is composed of the SubSeries listed below.
2015-12-30 | GSE68524 | GEO
Project description:Cardiomyocyte poly(A) RNA was sequenced from purified bulk cardiomyocytes collected from one male and female murine heart at postnatal day 2 (P2). Neonatal cardiomyocytes were isolated and purified (96% cardiomyocytes at P2) by Langendorff retrograde perfusion and immunomagnetic cell separation, respectively. We found evidence of sexual dimorphism with 9 differentially expressed genes (FDR<0.05) encoded on XY chromosomes in this RNA-Seq dataset.
2022-04-30 | GSE193137 | GEO
Project description:Whole transcriptome and miRNA analysis of neonatal mice hearts after myocardial infarction
| PRJNA814520 | 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 | GSE123863 | GEO
Project description:The adult mammalian heart is incapable of regeneration following injury. In contrast, the neonatal mouse heart has a transient ability to regenerate, however the molecular mechanism that mediates this regenerative response is not fully understood. Here, by single-nucleus RNA sequencing we map the transcriptome landscape of cardiomyocytes in neonatal mouse hearts at healthy, regenerative, and remodeling conditions. We show that an immature cardiomyocyte population enters cell-cycle in response to injury. Absence of this cardiomyocyte population overtime is associated with the loss of the ability of the heart to regenerate. We show a defined injury response in these cardiomyocytes, including activation of transcription factors NFYa and NFE2L1, which play proliferative and protective roles, respectively. We further show that overexpression of these two factors in vivo promotes heart regeneration. Thus, these findings refined our understanding of cellular basis of neonatal heart regeneration and reveal dynamic transcriptome landscape of cardiomyocytes in response to injury.
2020-03-18 | GSE142365 | GEO