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NEIL3 MI

ABSTRACT: Whole genome deep sequencing on DNA from non-infarcted left ventricle of WT and NEIL3-deficient mice subjected to myocardial infarction

PROVIDER: PRJEB17998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1736240_1.fastq.gz	Fastqsanger.gz
	ERR1736240_2.fastq.gz	Fastqsanger.gz
	ERR1736241_1.fastq.gz	Fastqsanger.gz
	ERR1736241_2.fastq.gz	Fastqsanger.gz

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Project description:Genome-wide analysis of gene expression in infarcted and non-infarcted left ventricle from NEIL3-deficient mice subjected to myocardial infarction

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Project description:Whole genome epigenetic sequencing on DNA from infarcted non-infarcted left ventricle of WT and NEIL3-deficient mice subjected to myocardial infarction

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RNA sequencing analysis of mouse cardiac endothelial cells in myocardial infarction tissues

Project description:To investigate the transcriotome alteration in endothelial cells (ECs) under a myocardial infarction (MI) condition, we performed RNA sequcening analysis with sorted ECs derived from mouse infarcted cardiac tissues or normal left ventricle (LV).

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Single-cell RNA sequencing analysis of mouse cardiac tissues with myocardial infarction

Project description:To investigate the transcriotome alteration in myocardial infarction (MI)-associated cells, we performed RNA sequcening analysis with single cells derived from mouse infarcted cardiac tissues or normal left ventricle (LV). Particularly, cardiac endothelial cells (ECs) were traced using a Cdh5-Cre;LSL-tdTomatom system.

2022-03-01 | GSE163956 | GEO

Transcriptomic profiling of chronic infarcted pig hearts

Project description:Myocardial infarction (MI) is the leading cause for hear failure (HF). Following MI, the non-infarcted region of left ventricle (LV) is critical for maintaining heart function, and disruption of the LV contributes greatly to post-MI HF. Transcriptomic profiling by high-throughput sequencing was performed in a chronic HF pig model, to explore the molecular changes in the post-MI LV related to cardiovascular deterioration. Samples were taken from heart tissue of MI-induced pigs and from control pigs not subjected to MI. Regions of the heart where samples were taken included the site of ischemia (LV ischemia), area bordering ischemia (LV border), area remote to ischemia (LV remote) and the right ventricle (RV).

2021-10-04 | E-MTAB-8856 | biostudies-arrayexpress

Genome-wide analysis of gene expression in infarcted and non-infarcted left ventricle from NEIL3-deficient mice subjected to myocardial infarction

Project description:Myocardial infarction (MI) triggers a reparative response involving fibroblast proliferation and differentiation driving extracellular matrix modulation necessary to form a stabilizing scar. Recently, it was shown that a genetic variant of the base excision repair enzyme endonuclease VIII-like 3 (NEIL3) was associated with increased risk of MI in humans. Here, we report elevated myocardial NEIL3 expression in heart failure patients and marked myocardial upregulation of Neil3 following MI in mice, especially in a fibroblast-enriched cell fraction. Neil3-/- mice showed increased mortality after MI compared to WT, caused by myocardial rupture. Neil3-/- hearts displayed enrichment of mutations in genes involved in mitogenesis of fibroblasts and transcriptome analysis revealed dysregulated fibrosis. Correspondingly, proliferation of vimentin+ and aSMA+ (myo)fibroblasts was increased in Neil3-/- hearts following MI. We propose that NEIL3 operates in genomic regions crucial for regulation of cardiac fibroblast proliferation and thereby controls extracellular matrix modulation after MI.

2016-11-01 | GSE83350 | GEO

Whole genome epigenetic sequencing on DNA from infarcted non-infarcted left ventricle of WT and NEIL3-deficient mice subjected to myocardial infarction

Project description:Myocardial infarction (MI) triggers a reparative response involving fibroblast proliferation and differentiation driving extracellular matrix modulation necessary to form a stabilizing scar. Recently, it was shown that a genetic variant of the base excision repair enzyme endonuclease VIII-like 3 (NEIL3) was associated with increased risk of MI in humans. Here, we report elevated myocardial NEIL3 expression in heart failure patients and marked myocardial upregulation of Neil3 following MI in mice, especially in a fibroblast-enriched cell fraction. Neil3-/-mice showed increased mortality after MI compared to WT, caused by myocardial rupture. Epigenomic analysis suggested dysregulated myofibroblast proliferation and differentiation in Neil3-/-hearts and several differentially expressed genes were downstream targets of differentially methylated/hydroxymethylated transcriptional regulators. Furthermore, proliferation of Vimentin+ and SMA+ (myo)fibroblasts was increased in Neil3 -/-hearts following MI. We propose that NEIL3-dependent modulation of epigenetic DNA methylation regulates cardiac fibroblast proliferation and thereby controls extracellular matrix modulation after MI.

2017-01-01 | GSE90057 | GEO

Transcriptional profiling of left ventricle and peripheral blood cells in rats with post-myocardial infarction

Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs) Myocardial infarction (MI) was induced in male Wistar rats by ligation of the proximal left coronary artery. The sham-operated group (control group) was subjected to the same protocol, except that the suture was not tied around the proximal left coronary artery. Sham-operated rats (n=6) and rats with small (n=6), moderate (n=6), and large (n=5) MI size were included into the experiment two months after the operation. Then, left ventricules and blood samples were obtained for RNA extraction and hybridization on Affymetrix microarrays. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals. The development of heart failure was estimated by echocardiography and catheterization.

2013-11-15 | E-GEOD-47495 | biostudies-arrayexpress

Transcription profiling of infarcted and non-infarcted left ventricles at different time points to study the molecular mechanism of myocardial infarction.

Project description:This dataset is a time series (1 hour [h], 4 hours, 24 hours, 48 hours, 1 week [w], and 8 weeks) intended to compare normal functioning left ventricles [lv + lv2] with infarcted [ilv] and non-infarcted left ventricles [nilv]. ilv samples are taken from the region between the LAD artery and the apex on a mouse with myocardial infarction. Lv2 samples are from the same region in a sham operated mouse. Nilv samples are taken from the region above the infartion and the left ventricle [lv] samples mimic that region in a sham mouse. The lv and lv2 samples can be compared as both are from normal functioning hearts. For more information visit http://cardiogenomics.med.harvard.edu/groups/proj1/pages/mi_home.html

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Expression data of Sham and post-MI myocardium from swine

Project description:The molecular mechanism underlying cardiac remodeling following myocardial infarction have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either sham surgery or permanent ligation of the left coronary artery (MI). RNA was isolated from the remote, non-ischemic, regions of the left ventricle.

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