Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of isolated neutrophils from Cd177 knockout mice post-SCI on microglia in a co-culture system

ABSTRACT: Effect of isolated neutrophils from Cd177 knockout mice post-SCI on microglia in a co-culture system

PROVIDER: PRJNA1157350 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30556980_1.fastq.gz	Fastqsanger.gz
	SRR30556980_2.fastq.gz	Fastqsanger.gz
	SRR30556981_1.fastq.gz	Fastqsanger.gz
	SRR30556981_2.fastq.gz	Fastqsanger.gz
	SRR30556982_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Effect of isolated neutrophils from Cd177 knockout mice post-SCI on microglia in a co-culture system

Project description:To investigate the transcriptional effects of CD177+ neutrophils on microglia in spinal cord injuries (SCI), we adapted a co-culture system containing isolated neutrophils from Cd177 WT or KO mice post-SCI and isolated microglia. Each group had a biological repeat (n=3).

2024-09-10 | GSE276429 | GEO

Effect of isolated neutrophils from Cd177 knockout mice post-SCI on macrophages in a co-culture system

Project description:To investigate the transcriptional effects of CD177+ neutrophils on macrophages in spinal cord injuries (SCI), we adapted a co-culture system containing isolated neutrophils from Cd177 WT or KO mice post-SCI and bone marrow-derived macrophages (BMDMs). Each group had a biological repeat (n=3).

2024-09-10 | GSE276427 | GEO

Effect of isolated neutrophils from Cd177 knockout mice post-SCI on macrophages in a co-culture system

Project description:Effect of isolated neutrophils from Cd177 knockout mice post-SCI on macrophages in a co-culture system

| PRJNA1157347 | ENA

CD177+ neutrophils to restrict neuroinflammation following CNS injury

Project description:Neutrophils are the most abundant circulating leukocyte population that play critical roles in neuroinflammation after ischemic stroke. CD177, a glycoprotein on neutrophils, is emerging as an important immune regulator which fundamentally affects multiple inflammatory diseases. However, the role and regulatory mechanism of CD177 protein of neutrophils in neuroinflammation remains elusive. Using single-cell RNA sequencing (scRNA-Seq), we characterized CD177high neutrophils as a novel anti-inflammatory subset in response to ischemic stroke.

2025-03-27 | GSE293098 | GEO

CD177+ neutrophils to restrict neuroinflammation following CNS injury

Project description:CD177+ neutrophils to restrict neuroinflammation following CNS injury

| PRJNA1242790 | ENA

Generation of pancreatic β cells from CD177+ anterior definitive endoderm

Project description:Methods for differentiating human pluripotent stem cells to pancreatic and liver lineages in vitro have been limited by the inability to identify and isolate distinct endodermal subpopulations specific to these two organs. Here we report that pancreatic and hepatic progenitors can be isolated using the surface markers CD177/NB1 glycoprotein and inducible T-cell costimulatory ligand CD275/ICOSL, respectively, from seemingly homogeneous definitive endoderm derived from human pluripotent stem cells. Anterior definitive endoderm (ADE) subpopulations identified by CD177 and CD275 show inverse activation of canonical and noncanonical WNT signaling. CD177+ ADE expresses and synthesizes the secreted WNT, NODAL and BMP antagonist CERBERUS1 and is specified toward the pancreatic fate. CD275+ ADE receives canonical Wnt signaling and is specified toward the liver fate. Isolated CD177+ ADE differentiates more homogeneously into pancreatic progenitors and into more functionally mature and glucose-responsive β-like cells in vitro compared with cells from unsorted differentiation cultures.

2020-04-27 | GSE113791 | GEO

Microglia coordinate cellular interactions during spinal cord repair

Project description:Traumatic spinal cord injury (SCI) triggers a neuro-inflammatory response dominated by tissue-resident microglia and monocyte derived macrophages (MDMs). Since activated microglia and MDMs are morphologically identical and express similar phenotypic markers in vivo, identifying injury responses specifically coordinated by microglia has historically been challenging. Here, we pharmacologically depleted microglia and use anatomical, histopathological, tract tracing, bulk and single cell RNA sequencing to reveal the cellular and molecular responses to SCI controlled by microglia. We show that microglia are vital for SCI recovery and coordinate injury responses in CNS-resident glia and infiltrating leukocytes. Depleting microglia exacerbates tissue damage and worsens functional recovery. Conversely, restoring select microglia-dependent signaling axes, identified through sequencing data, in microglia depleted mice prevents secondary damage and promotes recovery. Additional bioinformatics analyses reveal that optimal repair after SCI and likely other forms of neurological disease, might be achieved by co-opting key ligand-receptor interactions between microglia, astrocytes and MDMs.

2022-06-01 | GSE196928 | GEO

Permanently Re-programmed Microglia in Spinal Cord Injury Contribute to Functional Recovery

Project description:Microglia are resident myeloid cells of the central nervous system (CNS). Recently, single-cell RNA sequencing (scRNAseq) has enabled description of a disease-associated subtype of microglia (DAM) with a role in neurodegeneration and demyelination. In this study we use scRNAseq to investigate the temporal dynamics of immune cells harvested from the epicenter of traumatic spinal cord injury (SCI). As a consequence of SCI, homeostatic microglia undergo permanent transcriptional re-programming into a subtype of microglia with striking similarities to previoysly reported DAM as well as a distinct microglial state found during development. Using a microglia depletion model we showed that DAM in SCI are derived from homeostatic microglia and strongly enhance recovery of hind limb locomotor function following injury.

2021-12-24 | GSE142849 | GEO

Acutely isolated murine cortical astrocytes and microglia: Alzheimer's disease vs wildtype

Project description:Isolation of glia from Alzheimer's mice reveals inflammation andÂ dysfunction. Reactive astrocytes and microglia are associated with amyloid plaques in Alzheimer's disease (AD). Yet, not much is known about the molecular alterations underlying this reactive phenotype. To get an insight into the molecular changes underlying AD induced astrocyte and microglia reactivity, we performed a transcriptional analysis on acutely isolated astrocytes and microglia from the cortex of aged controls and APPswe/PS1dE9 AD mice. As expected, both cell types acquired a proinflammatory phenotype, which confirms the validity of our approach. Interestingly, we observed that the immune alteration in astrocytes was relatively more pronounced than in microglia. Concurrently, our data reveal that astrocytes display a reduced expression of neuronal support genes and genes involved in neuronal communication. The microglia showed a reduced expression of phagocytosis and/or endocytosis genes. Co-expression analysis of a human AD expression data set and the astrocyte and microglia data sets revealed that the inflammatory changes in astrocytes were remarkably comparable in mouse and human AD, whereas the microglia changes showed less similarity. Based on these findings we argue that chronically proinflammatory astrocyte and microglia phenotypes, showing a reduction of genes involved in neuronal support and neuronal signaling, are likely to contribute to the neuronal dysfunction and cognitive decline in AD. 2 cell types from 2 conditions: cortical microglia and cortical astrocytes from 15-18 month old APPswe/PS1dE9 mice compared to wildtype littermates. Biological replicates: microglia from APPswe/PS1dE9, N=7, microglia from WT, N=7, astrocytes from APPswe/PS1dE9, N=4, microglia from WT, N=4

2015-11-04 | E-GEOD-74615 | biostudies-arrayexpress

sci-ATAC-seq data

Project description:sci-ATAC-seq data

| PRJNA785974 | ENA