Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis of early changes in mouse heart transcriptome after myocardial infarction

ABSTRACT: Analysis of early changes in mouse heart transcriptome after myocardial infarction

PROVIDER: PRJNA412001 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6068402_1.fastq.gz	Fastqsanger.gz
	SRR6068402_2.fastq.gz	Fastqsanger.gz
	SRR6068403_1.fastq.gz	Fastqsanger.gz
	SRR6068403_2.fastq.gz	Fastqsanger.gz
	SRR6068404_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Analysis of early changes in mouse heart transcriptome after myocardial infarction

Project description:Alternative splicing of RNA is an underexplored area of transcriptional response. We hypothesized that early changes in alternatively spliced genes may be important for responses to cardiac injury. The goal of this study was to use high throughput sequencing to determine which genes undergo alternative splicing in the initial response to ischemia after myocardial infarction.

2018-05-07 | GSE104187 | GEO

Optimized alternative ordering of dapagliflozin and sacubitril-valsartan in post-myocardial infarction heart failure

Project description:We tested it in an animal model of myocardial infarction to ensure whether early initiation of dapagliflozin (DAPA), or different orders of combination with sacubitril-valsartan would result in a greater improvement of heart function than sacubitril-valsartan alone in post-myocardial infarction heart failure.

2023-04-13 | GSE229147 | GEO

Examination of mouse heart cell expression changes after myocardial Infarction

Project description:Examination of mouse heart cell expression changes after myocardial Infarction

| PRJNA638370 | ENA

myocardial infarction in Reg3beta knock-out mice

Project description:Affymetrix microarray analysis of molecular changes after myocardial infarction. Samples of heart tissue were analyzed after myocardial infarction from WT and reg3beta knock-out mice. Samples from scar tissue and samples adjacent to the scar were analyzed. In the experiment we primarily compared infarction zone of wild-type to infarction zone of knock-out animals, and remote zone of wild-type to remote zone of knock-outs.

2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Mouse Data)

Project description:We demonstrate an age-independent loss of type H bone endothelium in heart failure after myocardial infarction in both mice and in humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1 production partially prevents the post-myocardial infarction loss of type H vasculature in mice.

2021-05-13 | E-MTAB-10448 | biostudies-arrayexpress

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche (Human Data)

2021-05-11 | E-MTAB-10432 | biostudies-arrayexpress

Extracellular BRICK1 drives heart repair after myocardial infarction

Project description:Tissue repair after myocardial infarction entails a vigorous angiogenic response that mitigates scarring and worsening of heart function and may represent a therapeutic target. Angiogenesis in the infarct wound is guided by incompletely defined myeloid cell–endothelial cell interactions. Here we identify the myeloid cell-expressed 75‑amino acid microprotein BRICK1 (short name: BRK1) as an indispensable driver of postinfarction angiogenesis. As a subunit of the intracellular actin-regulatory WAVE complex, BRK1 was not previously known to function outside the cell. We show that BRK1 translocates to the extracellular space after myocardial infarction in mice and humans. We find that BRK1 is not actively secreted but released from dying monocytes and macrophages. Cre-loxP-mediated myeloid cell-selective genetic deletion of Brk1 or antibody neutralization of extracellular BRK1 impaired microvessel formation in the infarct border zone and resulted in severe postinfarction heart failure in mice. Treatment with recombinant BRK1, conversely, preserved heart function after myocardial infarction. Mechanistically, BRK1 induced an angiogenic phenotype in human cardiac endothelial cells by signaling via the small GTPase RAP1 and mitogen-activated protein kinases 1 and 3 to promote retinoblastoma protein hyperphosphorylation and E2F transcription factor activation. BRK1 thus emerges as an angiogenic growth factor linking myeloid cell death to ischemic tissue repair and potentially enabling a protein-based therapy for myocardial infarction.

2025-11-11 | GSE291736 | GEO

LncRNAs and mRNAs changes in border zone of myocardial infarction in rats

Project description:Comparison of both LncRNAs and mRNAs expression in the border zone of the myocardial infarction rats and the sham operation rats Border zone (BZ) of the myocardial infarction is critical to patients. Current treatments of myocardial infarction are primarily aimed to save the dying myocardial cell in the border zone. During myocardial infarction, certain changes in BZ, e.g, apoptosis, fibrosis, inflammation, etc, played an important role in deciding the survival. Impairment and recovery of BZ has been linked to gene expression changes. The aim of our study was to obtain a global expression profile of lncRNAs and mRNAs of the border zone in Wistar rats myocardial infarction, and identify the changes during myocardial infarction.

2016-12-02 | GSE90745 | GEO

Extracellular BRICK1 drives heart repair after myocardial infarction

Project description:Extracellular BRICK1 drives heart repair after myocardial infarction

| PRJNA1235165 | ENA

Examination of mouse heart cell expression changes after myocardial Infarction

Project description:The mammalian heart possesses a poor ability to regenerate after acute ischemic cardiac injury and lost cardiac muscle is replaced by scar tissue. Multiple clinical studies demonstrate that the size of scar tissue following myocardial infarction is an independent predictor of cardiovascular outcomes, yet little is known about factors that regulate the size of scar after ischemic cardiac injury. In this report, we demonstrate that collagen V, a fibrillar collagen and a minor constituent of heart scars regulates the size of heart scars after ischemic cardiac injury. Depletion of collagen V in heart scars in two independent animal models led to a significant and paradoxical increase in post infarction scar tissue size with worsening of heart function. A systems genetics approach analyzing genes versus traits across 100 in-bred strains of mice independently demonstrated that collagen V is a critical driver of post injury heart function. We show that collagen V deficiency alters the ultra-structure and mechanical properties of scar tissue that make it more vulnerable to expansion. There is altered reciprocal feedback between matrix and cells that induce expression of specific mechanosensitive integrins which drive fibroblast activation and increased ECM gene expression. Scar size increases. Administration of cilengitide, an inhibitor of specific integrins, completely rescues the phenotype of increased post injury scarring, myofibroblast formation and cardiac dysfunction in collagen V deficient mice. These observations demonstrate that collagen V, a structural constituent of heart scar tissue regulates scar size in an integrin dependent manner.

2020-06-10 | GSE152122 | 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