Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-MTAB-3149

ABSTRACT: Transcription profiling by array of rat hearts following myocardial infarction

DISEASE(S): Myocardial Infarction,Control

PROVIDER: E-MTAB-3149 | ExpressionAtlas | 2017-02-09

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-MTAB-3149-analysis-methods.tsv	Tabular
	E-MTAB-3149-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-3149-configuration.xml	Xml
	E-MTAB-3149-percentile-ranks.tsv	Tabular
	E-MTAB-3149.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 64

Similar Datasets

GPNMB Involved in Ischemic and Dilated Cardiac Diseases

Project description:A microarray-based screening was conducted in rat hearts 24 hours after myocardial infarction (MI) with the aim to discover yet unknown molecules that might have an impact on cardiac pathophysiology.

2015-06-30 | E-MTAB-3149 | biostudies-arrayexpress

Transcription profiling of Tbx1 function in adult myocardial infarction hearts [bulk RNA-seq]

Project description:Transcription profiling of Tbx1 function in adult myocardial infarction hearts [bulk RNA-seq]

| PRJNA564495 | ENA

Genome-wide analysis of gene expression changes in miR-214 KO mouse hearts and skeletal muscle

Project description:Early reperfusion of ischemic cardiac tissue remains the most effective intervention for improving clinical outcome following myocardial infarction. However, abrupt increases in intracellular Ca2+ during myocardial reperfusion cause cardiomyocyte death and consequent loss of cardiac function, referred to as ischemia/reperfusion (IR) injury. Cardiac IR is accompanied by dynamic changes in expression of microRNAs (miRNAs), which inhibit specific mRNA targets. miR-214 is up-regulated during ischemic injury and heart failure in mice and humans, but its potential role in these processes is unknown. We show that genetic deletion of miR-214 in mice causes loss of cardiac contractility, increased apoptosis, and excessive fibrosis in response to IR injury. The microarray contains 6 samples, each containing cDNA pooled from 3 mice per group. There are no replicates. The array was designed to make 3 different pairwise comparisons between the following: P14 WT and miR-214 KO hearts; adult WT and miR-214 KO skeletal muscle; adult WT and miR-214 KO hearts

2012-01-31 | E-GEOD-35421 | biostudies-arrayexpress

Targeting Immune-Fibroblast Crosstalk in Myocardial Infarction and Cardiac Fibrosis I

Project description:To define the cellular landscape of human myocardial infarction and heart failure, we performed Cellular Indexing of Transcriptomes and Epitomes by sequencing (CITE-seq) in 22 explanted human hearts from healthy donors, acute myocardial infarction (MI),and chronic ischemic and non-ischemic cardiomyopathy patients.

2024-07-01 | GSE217494 | GEO

Analysis of cardiac miRNA expression in the early neonatal period

Project description:The regenerative capacity of the mammalian heart is lost quickly after birth when cardiomyocytes stop dividing and undergo cell cycle arrest. Thus, the adult mammalian heart lacks the ability to heal itself to any appreciable amount after ischemic injury such as myocardial infarction. Heart growth begins during fetal life with the first phase of DNA synthesis that is exclusively associated with cardiomyocyte proliferation. This process proceeds until 12 hours after birth and is defined as 0 days in our submitted samples. Cardiomyocytes division is undetectable at neonatal day 1. To analyze the molecular mechanisms responsible for cessation of cardiomyocyte proliferation, we performed genome-wide miRNA microarray profiling by comparing postnatal days 0 vs 1d.This revealed a profile of 8 significantly downregulated miRNAs in the proliferative DKO hearts (versus vehicle-injected control), that were enriched for mRNA targets involved in cell cycle regulation. In vitro studies have demonstrated that knockdown of these 8 miRNAs in neonatal rat cardiomyocytes can increase the occurrence of cytokinetic events. Ultimately, we aim to inject antagomirs targeting these miRNAs into mice post-myocardial infarction to determine the effect of these miRNAs on heart function and cardiomyocyte proliferation in vivo.

2022-01-30 | E-MTAB-9256 | biostudies-arrayexpress

Gene expression profiles of hexadecyl-4-124I-iodobenzoate(124I-HIB)-labeled adipose-derived stem cells (ADSCs) in vitro and in vivo

Project description:[1] Microarray analysis in the rat myocardial tissue: 124I-HIB transplanted MI model Vs. phosphate buffered saline (PBS) injected myocardial infarction (MI) model Vs. Sham operated model [2] Microarray analysis in the rat adipose derived stem cells: 124I-HIB-labeled ADSCs Vs. Unlabeled ADSCs [1] We investigated the change of gene expression profile in sham operated-, PBS injected- and 124I-HIB-labeled ADSCs transplanted myocardium in rat myocaridial infarction (MI) model. [2] We compared gene expression profile with 124I-HIB labeled ADSCs and unlabeled ADSCs in vitro.

2015-01-06 | E-GEOD-64692 | biostudies-arrayexpress

Thrombopoietin (TPO) protects against heart damage induced infarction in rat model

Project description:In order to examine the mechanism of TPO on cardiac protection against myocardial infarction damage (MI), we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to delineate the TPO cardioprotective mechanism against infarction. MI and TPO induced gene expressions in rat heart were measured at week 4. Two biological replicates were performed for each treatment group.

2012-12-01 | E-GEOD-22489 | 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

Mus musculus

Project description:Expression data from C57BL/6J and MRL/MpJ hearts following acute myocardial infarction

| PRJNA120865 | ENA

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data