Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Spatially clustered type I interferon responses at injury borderzones [scRNA-Seq]

ABSTRACT: Spatially clustered type I interferon responses at injury borderzones [scRNA-Seq]

PROVIDER: PRJNA1119369 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29262105_1.fastq.gz	Fastqsanger.gz
	SRR29262105_2.fastq.gz	Fastqsanger.gz
	SRR29262106_1.fastq.gz	Fastqsanger.gz
	SRR29262106_2.fastq.gz	Fastqsanger.gz
	SRR29262107_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 50

Similar Datasets

Spatially clustered type I interferon responses at injury borderzones

Project description:Spatially clustered type I interferon responses at injury borderzones

| PRJNA1120028 | ENA

Spatially clustered type I interferon responses at injury borderzones [scRNA-Seq]

Project description:Sterile inflammation post-myocardial infarction was thought to be driven by myeloid cells, however, we show that borderzone cardiomyocytes are the critical initators of the Type I Interferon response through spatial, single-cell, and single-nuclei transcriptomics.

2024-08-06 | GSE268876 | 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

Spatially clustered type I interferon responses at injury borderzones.

Project description:Sterile inflammation after myocardial infarction is classically credited to myeloid cells interacting with dead cell debris in the infarct zone1,2. Here we show that cardiomyocytes are the dominant initiators of a previously undescribed type I interferon response in the infarct borderzone. Using spatial transcriptomics analysis in mice and humans, we find that myocardial infarction induces colonies of interferon-induced cells (IFNICs) expressing interferon-stimulated genes decorating the borderzone, where cardiomyocytes experience mechanical stress, nuclear rupture and escape of chromosomal DNA. Cardiomyocyte-selective deletion of 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. Interferons blunted the protective matricellular programs and contractile function of borderzone fibroblasts, and increased vulnerability to pathological remodelling. In mice that died after myocardial infarction, IFNIC colonies were immediately adjacent to sites of ventricular rupture, while mice lacking IFNICs were protected from rupture and exhibited improved survival3. Together, these results reveal a pathological borderzone niche characterized by a cardiomyocyte-initiated innate immune response. We suggest that selective inhibition of IRF3 activation in non-immune cells could limit ischaemic cardiomyopathy while avoiding broad immunosuppression.

| S-EPMC11374671 | biostudies-literature

Spatially clustered loci with multiple enhancers are frequent targets of HIV-1

Project description:Spatially clustered loci with multiple enhancers are frequent targets of HIV-1

| PRJNA554901 | ENA

Temporally & Spatially-Resolved Microproteomics and MALDI MSI Lipidomic Analysis for Traumatic Brain Injury

Project description:Using an experimental TBI rat model of mild/moderate Controlled Cortical Impact (CCI) injury, we combined large-scale proteomics identification and relative quantification using Spatially-Resolved Microproteomics with MALDI MS Imaging of Lipids. Spatially by studying different regions in the brain post injury in a coronal view, with main focus on the injury site itself. Temporally by studying the acute and subacute phase post injury, including injured rat brains at 1 day, 3 days, 7 days, and 10 days post injury. Direct on-tissue micro-digestion followed by micoextraction from 1 mm2 surface area within the injured cortical tissue were subjected to LC-MS & MS/MS analysis using HR MS. In addition, several identified potential biomarkers within our study were used to stimulate dorsal root ganglion (DRG), astrocyte, and macrophage cell lines to obtain a better understanding of their role and contribution in the injury.

2019-06-19 | PXD011262 | Pride

scRNA-seq time course of cerebellar Nestin-expressing progenitors from neonatal mice with and without injury at birth

Project description:To investigate the molecular changes that NEP subpopulations endure upon injury and to determine whether specific populations of NEPs have a transient increase in the signaling pathways associated with injury induced cellular stress and ROS, we performed multiplexed scRNA-seq of NEPs (CFP+) isolated by fluorescence activated cell sorting (FACS) from Nes-CFP/+ transgenic neonates with and without irradiation at timepoints P1, P2, P3 and P5.

2024-09-01 | E-MTAB-13353 | biostudies-arrayexpress

High resolution spatially resolved transcriptomic atlas of kidney injury and repair by RNA hybridization-based in situ sequencing [10X Visium]

Project description:Spatially resolved transcriptomics technologies allow for the measurement of gene expression in situ. We applied direct RNA hybridization-based in situ sequencing (ISS, Cartana) to compare male and female healthy mouse kidneys and the male kidneys injury and repair timecourse of ischemic reperfusion injury (IRI). A pre-selected panel of 200 genes were used to identify the dynamics of cell states and their spatial distributions during injury and repair. We developed a new computational pipeline, CellScopes, for the rapid analysis, multi-omic integration and visualization of spatially resolved transcriptomic datasets. The resulting atlas allowed us to resolve distinct kidney niches, dynamic alterations in cell state over the course of injury and repair and cell-cell interactions between leukocytes and kidney parenchyma. Projection of snRNA-seq dataset from the same injury and repair samples allowed us to impute the spatial localization of genes not directly measured by Cartana.

2024-01-17 | GSE227045 | GEO

High resolution spatially resolved transcriptomic atlas of kidney injury and repair by RNA hybridization-based in situ sequencing [ISS, Cartana]

2024-01-17 | GSE227044 | GEO

scRNA and snATAC sequencing of cells harvested from the tendon injury site after a severe burn/tenotomy injury

Project description:scRNA and snATAC sequencing of cells harvested from the tendon injury site after a severe burn/tenotomy injury in Hoxa11 lineage traced mice allowed for differentation tracing of MSCs located in zeugopod after severe heterotopic ossification inducing injury. The use of immobilization also allowed us to determine the effects of limb immoblization on MSCs during aberrant wound healing.

2020-06-30 | GSE150995 | 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