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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.

| S-EPMC7392272 | biostudies-literature

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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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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Whole transcriptome 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.

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Gene expression changes in beta-blocker treated neonatal hearts

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miRNA expression data from human myocardial infarction hearts

Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of human MI samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome Human tissue samples, acquired during post-mortem examination and frozen in liquid nitrogen, were provided by the department of pathology, Tokyo Metropolitan Geriatric Hospital after the approval from the ethical committee. Age- and sex-matched cohorts were selected to compare healthy hearts to those with post-MI LV remodeling. Border zone for myocardial infarction was sampled. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChipÂ® miRNA 3.0 Arrays

2016-01-07 | E-GEOD-76591 | biostudies-arrayexpress

microRNA data from mice hearts of 21 days post myocardial infarction versus sham control

Project description:microRNAs control cardiac remodeling post myocardial infarction, though the cellular and molecular mechanisms remain unclear. We used microarrays to examine microRNA profiles in mice hearts 21 days after ligation of left anterior descending coronary artery (LAD) versus sham control.

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

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| PRJNA449679 | ENA

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