Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single Nucleus ATAC Sequencing Reveals Epigenomic Regulation After Myocardial Infarction

ABSTRACT: Single Nucleus ATAC Sequencing Reveals Epigenomic Regulation After Myocardial Infarction

PROVIDER: PRJNA698968 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13613330.fastq.gz	Fastqsanger.gz
	SRR13613330_1.fastq.gz	Fastqsanger.gz
	SRR13613330_2.fastq.gz	Fastqsanger.gz
	SRR13613331.fastq.gz	Fastqsanger.gz
	SRR13613331_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Single Nucleus ATAC Sequencing Reveals Epigenomic Regulation After Myocardial Infarction

Project description:We generated a single cell accessibility atlas from different time points after murine myocardial infarction as an important source for the field.

2023-02-01 | GSE166008 | GEO

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

Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction

Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.

2014-10-23 | E-GEOD-62646 | biostudies-arrayexpress

The Myocardial Infarction Platelet Transcriptome

Project description:The Myocardial Infarction Platelet Transcriptome

| PRJNA1135265 | ENA

Myocardial Infarction accelerates breast cancer via innate immune reprogramming (ATAC-seq)

Project description:Myocardial Infarction accelerates breast cancer via innate immune reprogramming (ATAC-seq)

| PRJNA573073 | ENA

CCR2+ monocytes promote white matter injury and cognitive dysfunction after myocardial infarction

Project description:Survivors of myocardial infarction are at increased risk for vascular dementia. Neuroinflammation has been implicated in the pathogenesis of vascular dementia, yet little is known about the cellular and molecular mediators of neuroinflammation after myocardial infarction. Using a mouse model of myocardial infarction coupled with flow cytometric analyses and immunohistochemistry, we discovered increased monocyte abundance in the brain after myocardial infarction, which was associated with increases in brain-resident perivascular macrophages and microglia. Myeloid cell recruitment and activation was also observed in post-mortem brains of humans that died after myocardial infarction. Spatial and single cell transcriptomic profiling of brain-resident myeloid cells after experimental myocardial infarction revealed increased expression of monocyte chemoattractant proteins. In parallel, myocardial infarction increased crosstalk between brain-resident myeloid cells and oligodendrocytes, leading to neuroinflammation, white matter injury, and cognitive dysfunction. Inhibition of monocyte recruitment preserved white matter integrity and cognitive function, linking monocytes to neurodegeneration after myocardial infarction. Together, these preclinical and clinical results demonstrate that monocyte infiltration into the brain after myocardial infarction initiate neuropathological events that lead to vascular dementia.

2025-05-21 | GSE268156 | 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

CCN3 administration after surgically induced myocardial infarction

Project description:CCN3 administration after surgically induced myocardial infarction

2023-02-27 | GSE217925 | GEO

Ckmt2 for Evaluating Reperfusion Injury in Acute Myocardial Infarction

Project description:Mitochondrial Creatine Kinase 2 (Ckmt2) as a Plasma-Based Biomarker for Evaluating Reperfusion Injury in Acute Myocardial Infarction

2024-10-17 | PXD055738 | Pride

Serial transcriptomic analysis of mouse acute myocardial infarction

Project description:Serial transcriptomic analysis of mouse acute myocardial infarction

2022-03-01 | GSE183272 | GEO