Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

ABSTRACT: Our study comprehensively investigated the epigenetic features of cardiac F4/80+CD45+ macrophages at 3 and 7 days after P1 and P10 MI at infarct, border, and remote zones of mouse hearts (IZ, BZ, and RZ) through single cell H3K27ac ChIP-seq. we identified 9 subclusters and analyzed their potential functions, cluster-specific enhancer features, and enrichment of cell-type specific transcription factors. Surprisingly, we found intracluster epigenetic heterogeneity exists with biological functions. Moreover, we identified two MI-responsive lineages and targeted one inflammatory lineage exhibiting obvious pre-regenerative function.

ORGANISM(S): Mus musculus

PROVIDER: GSE225615 | GEO | 2024/09/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Single Cell Spatial Transcriptomics Redefines the Borderzone induced by Myocardial Infarction and Mechanical Injury

Project description:The ischemic borderzone (BZ) is a geographically complex and biologically enigmatic interface separating poorly perfused infarct zones (IZ) from comparatively healthy remote zones (RZ). BZ cellular and molecular mechanisms are not well understood because efforts to dissect it inevitably include RZ and IZ in uncontrolled proportions. Here, we use single-cell/nuclei RNA-sequencing, spatial transcriptomics, and multiplexed RNA fluorescence in situ hybridization (mFISH) to identify BZ cardiomyocytes (CMs) subsets. BZ1 (Nppa+Xirp2-) forms a hundreds-of-microns-thick transitional layer adjacent to RZ, while BZ2 (Nppa+Xirp2+) forms a tens-of-microns-thick layer that the IZ edge. BZ2 CMs have reduced CM cell contact; colocalize with matricellular-protein-expressing myofibroblasts; and upregulate focal adhesion-, sarcomere-, and cytoskeletal-genes. Surprisingly, the transcriptional BZ emerges within an hour of injury and is inducible by non-ischemic fine-needle-trauma. We suggest that mechanical instability and “loss of neighbor” at the BZ edge are the dominant inducers of the BZ transcriptional response.

2022-10-03 | GSE214611 | GEO

Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

Project description:Our study comprehensively investigated the epigenetic features of cardiac F4/80+CD45+ macrophages at 3 and 7 days after P1 and P10 MI at infarct, border, and remote zones of mouse hearts through single cell H3K27ac ChIP-seq. we identified 9 subclusters and analyzed their potential functions, cluster-specific enhancer features, and enrichment of cell-type specific transcription factors. Surprisingly, we found intracluster epigenetic heterogeneity exists with biological functions. Moreover, we identified two MI-responsive lineages and targeted one inflammatory lineage exhibiting obvious pre-regenerative function.

2024-09-06 | GSE235275 | GEO

Epicardial Placement of Human Placental Membrane Protects from Heart Injury in a Swine Model of Myocardial Infarction

Project description:Introduction: Cardiac ischemic reperfusion injury (IRI) is paradoxically instigated by re-establishing blood-flow to ischemic myocardium typically from a myocardial infarction (MI). Although revascularization following MI remains the standard of care, effective strategies remain limited to prevent or attenuate IRI. We hypothesized that epicardial placement of human placental amnion/chorion (HPAC) grafts will protect against IRI. Methods: Using a clinically relevant model of IRI, swine were subjected to 45 minutes percutaneous ischemia followed with (MI+HPAC, n=3) or without (MI only, n=3) HPAC. Cardiac function was assessed by echocardiography, and regional punch biopsies were collected 14 days post-operatively. A deep phenotyping approach was implemented by using histological interrogation and incorporating global proteomics and transcriptomics in non-ischemic, ischemic, and border zone biopsies. Results: Our results established HPAC limited the extent of cardiac injury by 50% (11.02.0% vs 22.03.0%, p=0.039) and preserved ejection fraction in HPAC-treated swine (46.8±2.7% vs 35.8±4.5%, p=0.014). We present comprehensive transcriptome and proteome profiles of infarct (IZ), border (BZ), and remote (RZ) zone punch biopsies from swine myocardium during the proliferative cardiac repair phase 14 days post-MI. Both HPAC-treated and untreated tissues showed regional dynamic responses, whereas only HPAC-treated IZ revealed active immune and extracellular matrix remodeling. Decreased endoplasmic reticulum (ER)-dependent protein secretion and increased anti-apoptotic and anti-inflammatory responses were measured in HPAC-treated biopsies. Discussion: We provide quantitative evidence HPAC reduced cardiac injury from MI in a preclinical swine model, establishing a potential new therapeutic strategy for IRI.

2023-05-30 | GSE228096 | GEO

Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

Project description:Our study comprehensively investigated the epigenetic features of cardiac F4/80+CD45+ macrophages after adult mouse MI or Sham sugery at infarct zones of mouse hearts through single cell H3K27ac ChIP-seq. We identified 7 subclusters and analyzed their potential functions, cluster-specific enhancer features.

2024-09-06 | GSE263798 | GEO

Spatially clustered type I interferon responses at injury borderzones

Project description:Sterile inflammation after myocardial infarction (MI) is classically credited to myeloid cells interacting with dead cell debris in the infarct zone (IZ). Here, we show that borderzone cardiomyocytes are the dominant initiators of a novel type I interferon (IFN) response in the infarct borderzone zone (BZ). Using spatial transcriptomics analysis of mice and humans, we find that MI induces colonies of interferon induced cells (IFNICs) expressing interferon stimulated genes (ISGs) decorating the BZ, where cardiomyocytes experience mechanical stress, nuclear rupture, and escape of chromosomal DNA. Cardiomyocyte-selective deletion of interferon regulatory factor 3 (Irf3) abrogated IFNIC colonies, whereas mice lacking Irf3 in fibroblasts, macrophages, neutrophils, or endothelial cells; Ccr2-deficient mice; or plasmacytoid dendritic cell-depleted mice did not. IFNs blunted the protective matricellular programs and contractile function of BZ fibroblasts, and increased vulnerability to pathologic remodeling. In mice that died after MI, IFNIC colonies were immediately adjacent to sites of ventricular rupture, while mice lacking IFNICs were protected from rupture and exhibited improved survival. Together, these results reveal a pathologic BZ niche characterized by a cardiomyocyte-initiated innate immune response. We suggest that selective inhibition of Irf3 activation in non-immune cells of the borderzone could limit ischemic cardiomyopathy while avoiding broad immunosuppression.

2024-08-06 | GSE269054 | GEO

8e35dae3-3022-40ca-b0c5-78b864825032 - samples

Project description:We applied an integrative single-cell genomics strategy with single nucleus RNA sequencing (snRNA-seq) and single nucleus Assay for Transposase-Accessible Chromatin sequencing (snATAC-seq) together with spatial transcriptomics from the same tissue mapping human cardiac cells in homeostasis and after myocardial infarction (MI) at unprecedented spatial and molecular resolution. We profiled in total 31 samples from 23 patients including four non-transplanted donor hearts as controls and samples from tissues with necrotic tissue areas (ischemic zone, IZ), border zone (BZ), and the non-affected left ventricular myocardium (remote zone, RZ) of patients with acute MI.

| EGAD00001008952 | EGA

Gene expression data from myocardial infarction porcine samples

Project description:The use of cDNA microarrays has made it possible to analyze expression of thousands of genes simultaneously. We employed microarray gene expression profiling of porcine cDNA to compare myocardial gene expression in infarct core and remote myocardium at 1 week (n=3), 4 weeks (n=3), and 6 weeks (n=3) after surgically induced myocardial infarction (MI) and in sham-operated controls (n=3). More than 8,000 cDNA sequences were identified in myocardium that showed differential expression in response to MI. Different temporal and spatial patterns of gene expression were recognized in the infarct core tissue within this large set of data. Microarray gene profiling revealed candidate genes, some of them described for the first time, which elucidate changes in biological processes at different stages after MI. We evaluated temporal gene expression in a porcine model of myocardial infarction by microarray technology. Nine female pigs (Sus scrofa crossbreed Landrace x Large White) weighing 30-40 kg were subjected to experimental MI by a double-ligation of the first marginal branch of the circumflex artery. Animals were randomly sacrificed at 1 week (n=3), 4 weeks (n=3), or 6 weeks (n=3) after MI. Three paired myocardial samples from the infarct core and remote myocardium were analyzed at each time point. Myocardial samples from sham-operated animals (open-chest cardiac exposure without coronary artery ligation; n=3) were included as physiological controls.

2013-03-01 | E-GEOD-34569 | biostudies-arrayexpress

Gene expression data from myocardial infarction porcine samples

2013-03-01 | GSE34569 | GEO

Expression data from C57BL/6J and MRL/MpJ hearts following acute myocardial infarction

Project description:The Murphy Roth Large (MRL) mouse, a strain capable of regenerating right ventricular myocardium, has a high post-myocardial infarction (MI) survival rate compared with C57BL6/J (C57) mice. The biological processes responsible for this survival advantage are unknown. We compared acute post-MI gene expression in C57 and MRL hearts using microarrays and identified promising candidate biological processes underlying increased survival in the MRL. Hearts from both strains were excised at different time points before or after MI for RNA extraction and hybridization to MOE430A arrays. Baseline hearts were excised from healthy mice that had not undergone the MI procedure (day 0). Infarct tissue in this case means tissue taken from the anterior-apical region that would be the infarct region in a post-MI heart. Non-infarct covers the remainder of the LV. Post-MI hearts were excised either 1 or 5 days after MI. We had successful hybridizations for 3 replicates each of C57 day 0 infarct and non-infarct tissue (6 arrays), 4 MRL day 0 infarct and non-infarct tissue (8 arrays), 4 C57 day 1 infarct and non-infarct tissue (8 arrays), 4 MRL day 1 infarct and non-infarct tissue (8 arrays), 4 C57 day 5 infarct and non-infarct tissue (8 arrays), and 4 MRL day 5 infarct and non-infarct tissue (8 arrays).

2010-05-27 | E-GEOD-19322 | biostudies-arrayexpress

label-free LC-MS/MS on heart tissues in ovine model of non-transmural infarcts

Project description:label-free relative quantitation based on nLC-MS/MS performed on heart tissues in a clinically relevant ovine model of non-transmural infarcts. Each of the seven samples (7d MI IS, 7d MI BZ, 7d MI FAR, 28d MI IS, 28d MI BZ, 28d MI FAR e HLT) has been analysed in two technical replicates.

2022-06-01 | MSV000089576 | MassIVE

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