Single Nucleus ATAC Sequencing Reveals Epigenomic Regulation After Myocardial Infarction
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE166008 | GEO | 2023/02/01
REPOSITORIES: GEO
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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
Project description:Single Nucleus ATAC Sequencing Reveals Epigenomic Regulation After Myocardial Infarction
| PRJNA698968 | ENA
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
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
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
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
Project description:CCN3 administration after surgically induced myocardial infarction
2023-02-27 | GSE217925 | GEO
Project description:Myocardial infarction (MI), the most severe manifestation of coronary artery disease, is a multifactorial pathophysiologic process. Here, we constructed a MI mouse model through ligation of the proximal left anterior descending coronary artery. Then we detected and analysed multi-omics (transcriptome and proteome) at different time points (Control, 10 mininte, 1 hour, 6 hour, 24 hour and 72 hour) after MI. Immune-related pathway, pyroptosis pathway, and autophagy pathway r were significantly increased after MI.
2021-09-14 | GSE153494 | GEO
Project description:Serial transcriptomic analysis of mouse acute myocardial infarction
2022-03-01 | GSE183272 | GEO
Project description:To further search for potential gene targets which are involved in the pathological process of myocardial infarction, we have employed whole genome microarray expression profiling as a discovery platform to identify the expression of STAT6, β1-adrenergic receptors and inflammatory cytokines. The CD11b+ cells were isolated from spleen and bone marrow of mice by magnetic beads, and the experimental mice were divided into four time points (control, MI 1week, MI 2 weeks, and MI 4 weeks). We found the β1-AR related sympathetic signal, the STAT6 signal and inflammatory cytokines (IL-1α, IL-18 and TGF-β) are involved in the activation of CD11b+ immune cells and cardiac fibrogenesis after myocardial infarction.
2020-11-16 | GSE154733 | GEO