Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Whole transcriptome analysis of neonatal mice hearts after myocardial infarction

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE198300 | GEO | 2022/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

miRNA analysis of neonatal mice hearts after myocardial infarction

2022-12-31 | GSE198301 | GEO

Accumulation of acylcarnitines and mitochondrial dysfunction characterize the loss of neonatal myocardial regeneration capacity

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 metabolic 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 (MI) and acute ischemic heart failure. Myocardial tissue samples were collected after 21 days for metabolomics, transcriptomics and proteomics analyses. Phenotypic characterizations were carried out using echocardiography, histology as well as mitochondrial structural and functional measurements. By integrating the findings from metabolome and transcriptome examinations, we identified mitochondrial dysfunction at the level of the carnitine shuttle contributing to myocardial regeneration incompetence. Regeneration failure was linked to accumulation of acylcarnitines and insufficient metabolic capacity for fatty acid beta-oxidation. We further identified specific transcription factors and post-transcriptional regulation contributing to both regeneration competence and failure. Rather than shifting from the preferred myocardial oxidative fuel source, our results put forward the facilitation of mitochondrial fatty acid transport and improving the beta- oxidation pathway to overcome the metabolic barriers for repair and regeneration in adult mammals after MI and heart failure.

2022-02-04 | MSV000088783 | MassIVE

Single-cell RNA sequencing data from murine hearts after infarction with Collagen-2 tracing

Project description:Data set contains samples from isolated cells of murine hearts after myocardial infarction (LAD surgery). We used Col1a2 tracing system to mark Collagen expressing cells within d3 to d7 post infarct. In brief, adult Col1a2-ERT2+/-;mT/mG mice, at an age of 12 weeks (n=4) as well as aged animals with 88-91 weeks (n=4) were used. Left anterior descending coronary artery ligation surgery was performed, inducing myocardial infarction. Homeostasis animals were not operated. For Cre induction we injected 2mg Tamoxifen from d3 to d7 post surgery. All animals were sacrificed 28d post injury. Murine scRNA-seq libraries were prepared using Chromium Single Cell 3′ v3 Reagent Kit (10X Genomics), according to manufacturer’s protocols. Raw reads were mapped against a customized version of mm10 (GRCm38.p4) containing sequences of EGFP and tdTomato.

2020-12-15 | E-MTAB-9817 | 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.

2017-02-12 | GSE74135 | GEO

Molecular alterations following myocardial infarction in mice

Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. To address this issue, we have performed microarray analysis of non-infarcted left ventricular tissue from mice at various time-points after myocardial infarction. Methods: Molecular alterations in myocardial tissue were measured 3, 5, 7 and 14 days after induced infarction by using cDNA microarrays. Sham operated mice served as controls. Altered gene transcriptions were verified by real-time polymerase chain reaction. Attention focused on genes encoding cytokines which had not previously been assigned a role in heart failure development. Results: The highest number of regulated genes was found at day 5 post myocardial infarction, and 22 genes encoding cytokines were identified as being regulated. Several of the identified genes encoding cytokines have not previously been associated with HF, and among those fractalkine showed strongest up-regulation. Keywords: Disease state analysis, time course

2008-09-25 | GSE6580 | GEO

mRNA Expression data from murine hearts subjected to ligation of the left anterior descending coronary artery (myocardial infarction, MI model) or sham surgery (SH)

Project description:The left anterior descending coronary artery permanent ligation model of myocardial infarction was used to study the time of day differences in genetic responses post-MI between sleep-time MI, wake-time MI, wake-sham and sleep-sham mouse hearts. The micorarray approach allows the investigation of gene expression changes of all genes in sleep-time MI vs. wake-time MI vs. sham hearts.

2018-08-06 | GSE71906 | 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

miRNA expression data from the hearts of murine myocardial infarction model

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. Similar observations have been reported in murine model of MI. 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 murine MI model samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome The left anterior descending (LAD) coronary artery of mice aged 10 weeks was surgically ligated to create extensive MI. The ventricular septum of the areas at risk of ischemia was sampled on post-operative day 28. 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-76592 | biostudies-arrayexpress

Single-cell RNA sequencing data from murine hearts after infarction with endothelial tracing

Project description:Data set contains samples from isolated cells of murine hearts after myocardial infarction (LAD surgery). We used an endothelial tracing system to mark endothelial cells with EGFP prior to infarct. In brief, Cdh5-ERT2+/-;mT/mG mice, which were used at an age of 10-12 weeks. Cre expression was induced by daily intraperitoneal injections of 2 mg tamoxifen for 1 week in all mice. One week after tamoxifen injection, left anterior descending coronary artery ligation surgery was performed, inducing myocardial infarction. We collected samples at homeostasis, days(d) 1, 3, 7, 14 and 28 after infarction and isolated the non-cardiomyocyte fraction for single cell sequencing. Murine scRNA-seq libraries were prepared using Chromium Single Cell 3′ v3 Reagent Kit (10X Genomics), according to manufacturer’s protocols. Raw reads were mapped against a customized version of mm10 (GRCm38.p4) containing sequences of EGFP and tdTomato.

2020-12-15 | E-MTAB-9816 | biostudies-arrayexpress

Evaluating the effects of cardiac telomerase re-activation after myocardial infarction in adult mice

Project description:Coronary heart disease is a main cause of death in the developed world and treatment success remains modest with high mortality rates within one year after myocardial infarction (MI). Thus, new therapeutic targets and effective treatments are necessary. Short telomeres are risk factors for age-associated diseases including heart disease. Here, we address the potential of telomerase (Tert) activation in prevention of heart failure after MI in adult mice. We use adeno-associated viruses for cardiac-specific Tert expression in a mouse model of MI. We find that upon MI, hearts expressing Tert show attenuated cardiac dilation, improved ventricular function and smaller infarct scars concomitant with increased mouse survival by 17% compared to controls. Furthermore, Tert treatment results in elongated telomeres, increased numbers of Ki67 and pH3-positive cardiomyocytes and a gene expression switch towards a regeneration signature of neonatal mice. Our work highlights telomerase activation as a novel therapeutic strategy to prevent heart failure after MI. Mice of one year of age were left untreated (control) or injected with 5*10^11 adeno associated viruses particles of serotype 9 (AAV9) that carry either en empty expression cassette or express telomerase under control of the CMV promoter. Virus injected mice then underwent myocardial infarction induced through permenant left anterior descending artery (LAD) ligation. Mice that survived for six weeks after LAD ligation were sacrificed and 4 hearts per group (AAV9-empty or AAV9-Tert) and 3 control hearts (no virus treatment, no ligation) were subjected to total RNA isolation for micro array analysis.

2014-12-15 | E-GEOD-62973 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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