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Identifying the Key Regulators that Promote Cell-cycle Activity in the Hearts of Early Neonatal Pigs after Myocardial Injury

ABSTRACT: Identifying the Key Regulators that Promote Cell-cycle Activity in the Hearts of Early Neonatal Pigs after Myocardial Injury

PROVIDER: PRJNA605206 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11039316_1.fastq.gz	Fastqsanger.gz
	SRR11039316_2.fastq.gz	Fastqsanger.gz
	SRR11039317_1.fastq.gz	Fastqsanger.gz
	SRR11039317_2.fastq.gz	Fastqsanger.gz
	SRR11039318_1.fastq.gz	Fastqsanger.gz

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Identifying the Key Regulators that Promote Cell-cycle Activity in the Hearts of Early Neonatal Pigs after Myocardial Injury

Project description:This is the dataset used in the paper: Zhang et al. Identifying the Key Regulators that Promote Cell-cycle Activity in the Hearts of Early Neonatal Pigs after Myocardial Injury. PloS One.

2020-02-07 | GSE144883 | GEO

Identifying the key regulators that promote cell-cycle activity in the hearts of early neonatal pigs after myocardial injury.

Project description:Mammalian cardiomyocytes exit the cell cycle shortly after birth. As a result, an occurrence of coronary occlusion-induced myocardial infarction often results in heart failure, postinfarction LV dilatation, or death, and represents one of the most significant public health morbidities worldwide. Interestingly however, the hearts of neonatal pigs have been shown to regenerate following an acute myocardial infarction (MI) occuring on postnatal day 1 (P1); a recovery period which is accompanied by an increased expression of markers for cell-cycle activity, and suggests that early postnatal myocardial regeneration may be driven in part by the MI-induced proliferation of pre-existing cardiomyocytes. In this study, we identified signaling pathways known to regulate the cell cycle, and determined of these, the pathways persistently upregulated in response to MI injury. We identified five pathways (mitogen associated protein kinase [MAPK], Hippo, cyclic [cAMP], Janus kinase/signal transducers and activators of transcription [JAK-STAT], and Ras) which were comprehensively upregulated in cardiac tissues collected on day 7 (P7) and/or P28 of the P1 injury hearts. Several of the initiating master regulators (e.g., CSF1/CSF1R, TGFB, and NPPA) and terminal effector molecules (e.g., ATF4, FOS, RELA/B, ITGB2, CCND1/2/3, PIM1, RAF1, MTOR, NKF1B) in these pathways were persistently upregulated at day 7 through day 28, suggesting there exists at least some degree of regenerative activity up to 4 weeks following MI at P1. Our observations provide a list of key regulators to be examined in future studies targeting cell-cycle activity as an avenue for myocardial regeneration.

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miRNA analysis of neonatal mice hearts after myocardial infarction

Project description:miRNA analysis of neonatal mice hearts after myocardial infarction

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Characterization of myocardial B cells in naïve hearts, acutely injured hearts and acutely injured hearts of mice treated with Pirfenidone

Project description:Myocardial CD19+CD11b+ and CD19+CD11b- cells were FACS sorted from transgenic mice expressing the Diphtheria Toxin (DT) receptor under the myocardial specific MLC2v promoter. Cells were sorted from hearts of mice not exposed to DT (naïve hearts), from the hearts of animals treated with DT 4 days prior to the experiment (DTR) and from the hearts of mice exposed to DT and fed chow enriched with the anti-inflammatory/anti-fibrotic drug Pirfenidone (0.5% in powdered chow, PFD)

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Whole transcriptome analysis of neonatal mice hearts after myocardial infarction

Project description:Whole transcriptome analysis of neonatal mice hearts after myocardial infarction

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miRNA analysis of neonatal mice hearts after myocardial infarction

Project description:Myocardial regeneration capacity declines during the first week after birth and is linked to the adaptation to oxidative metabolism. Utilizing this regenerative window, we characterized the transcriptomic changes in myocardial injury in 1-day-old regeneration-competent and 7-day-old regeneration-compromised mice. The mice were either sham-operated or received left anterior descending coronary artery ligation to induce myocardial infarction and acute ischemic heart failure. Myocardial tissue samples were collected after 3- and 21-day follow-up period. Whole transcriptome and miRNA NGS data was analyzed. We identified specific time-dependent transcription factors and networks contributing to both regeneration competence and failure.

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Project description:Whole transcriptome and miRNA analysis of neonatal mice hearts after myocardial infarction

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Site-specific N-glycan Analysis of Neonatal Mouse Hearts

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

Gene expression changes in beta-blocker treated neonatal hearts

Project description:The regeneration potential of the mammalian heart is limited. We found that treatment of beta-blocker robustly enhanced cardiomyocyte proliferation and promoted cardiac regeneration post myocardial infarction. To investigate the gene expression changes, we performed RNA-seq using the hearts treated with beta-blocker for 7 days.

2022-08-30 | GSE186099 | GEO

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