Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Card9 knockout on gene expression in cardiac tissues of mice post myocardial infarction

ABSTRACT: Effect of Card9 knockout on gene expression in cardiac tissues of mice post myocardial infarction

PROVIDER: PRJNA985628 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24976873.fastq.gz	Fastqsanger.gz
	SRR24976874.fastq.gz	Fastqsanger.gz
	SRR24976875.fastq.gz	Fastqsanger.gz
	SRR24976876.fastq.gz	Fastqsanger.gz
	SRR24976877.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Effect of Card9 knockout on gene expression in cardiac tissues of mice post myocardial infarction

Project description:Immune cell infiltration in response to myocyte death contributes to extracellular matrix (ECM) remodeling and scar formation after myocardial infarction (MI). Caspase-recruitment domain protein 9 (CARD9) which belongs to CARD family acts as an adapter that mediate the transduction of proinflammatory signaling cascades in innate immunity. To investigate the role of CARD9 in cardiac injury and repair post ischemia, we subjected Card9 knockout mice to myocardial infarction (MI) , and then performed RNA-seq and gene expression profiling analysis using the ischemic cardiac tissues at 3 days post-MI, to identify key genes and pathways regulated by CARD9.

2023-10-25 | GSE235257 | GEO

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

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).

2021-12-31 | GSE163772 | GEO

Cardiac organoid model of human myocardial infarction

Project description:Cardiac organoid model of human myocardial infarction

| PRJNA454314 | ENA

Single-cell RNA-seq of mouse cardiac interstitial cells 3 & 7 days after sham or myocardial infarction injury

Project description:The aims of the experiment were to profile the cell types in the adult mouse cardiac interstitium (non-myocyte cells) and how they respond to myocardial infarction injury. Adult, male, Pdgfra +/GFP mice were subject to either a myocardial infarction or sham injury, with cells isolated from cardiac ventricles 3 or 7 days following surgery. We obtained scRNA-seq profiles of two cell fractions: total interstitial (non-myocyte) cell population (TIP) and FACS-sorted GFP+/Cd31- cells (GFP).

2019-03-28 | E-MTAB-7376 | biostudies-arrayexpress

Cardiac organoid model of human myocardial infarction (batch2)

Project description:Cardiac organoid model of human myocardial infarction (batch2)

| PRJNA473541 | ENA

Cardiac organoid model of human myocardial infarction

Project description:While human organoid systems have provided a powerful platform in modeling diseases caused by genetic disorders, non-genetic factors, such as lifestyle and environment, are the largest attributable factors to devastating diseases like cardiovascular disease (CVD), the leading cause of death worldwide. Specifically, myocardial infarction (MI) (i.e., heart attack) makes up ~8.5% of CVD and is a common cause of heart failure with a 40% five-year mortality after the first MI. This highlights an urgent need to develop relevant human heart failure models for drug development. This is further evidenced by the disappointing performance of heart failure drugs in clinical trials during the last decade, which has been partially attributed to the distinct differences between human patient hearts and animal heart failure models. Here, we combined major non-genetic causal factors of MI with our previously established cardiac organoids to create the first human organoid model of cardiac infarction. In particular, we leveraged the diffusion limitation in 3D microtissues to recreate the nutrient diffusion gradient across infarcted hearts (i.e., infarct-border-remote zones) in human cardiac organoids to induce cardiac organotypic response to infarction. This enabled the recapitulation of major MI hallmarks in human cardiac organoids at the transcriptomic, structural and functional level.

2020-04-14 | GSE113871 | GEO

Mouse Cardiac Fibroblasts post MI

Project description:Analysis of one-day cultured cardiac fibroblasts after acute myocardial infarction

2020-05-20 | MSV000085454 | MassIVE

Cardiac organoid model of human myocardial infarction (batch2)

2020-04-14 | GSE115031 | GEO

Spatial multi-omic map of human myocardial infarction

Project description:Myocardial infarction is a leading cause of mortality worldwide 1 . While advances have been made in acute treatment, an incomplete understanding of remodelling processes has limited the effectiveness of therapies to reduce late-stage mortality 2 . Here, we generate an integrative high- resolution map of human cardiac remodelling after myocardial infarction using single-cell gene expression, chromatin accessibility, and spatial transcriptomic profiling of multiple physiological zones at distinct time points in myocardium from myocardial infarction and control patients. Multimodal data integration allowed us to evaluate cardiac cell-type compositions at increased resolution, yielding insights into changes of the cardiac transcriptome and epigenome through the identification of distinct tissue structures of injury, repair and remodelling. We identified and validated disease-specific cardiac cell-states of major cell-types and analysed them in their spatial context, evaluating their dependency on other cell-types. Our data elucidates molecular principles of human myocardial tissue organisation, recapitulating a gradual cardiomyocyte and myeloid continuum following ischemic injury. In total, our study provides an integrative molecular map of human myocardial infarction and represents an essential reference for the field and paves the way for advanced mechanistic and therapeutic studies of cardiac disease.

| EGAS00001006330 | EGA

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