Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile of microglia and border-associated macrophages carrying hDNMT3A mutation

ABSTRACT: Gene expression profile of microglia and border-associated macrophages carrying hDNMT3A mutation

PROVIDER: PRJNA1187610 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31384770_1.fastq.gz	Fastqsanger.gz
	SRR31384770_2.fastq.gz	Fastqsanger.gz
	SRR31384771_1.fastq.gz	Fastqsanger.gz
	SRR31384771_2.fastq.gz	Fastqsanger.gz
	SRR31384772_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 56

Similar Datasets

Gene expression profile of microglia and border-associated macrophages carrying hDNMT3A mutation

Project description:To probe for the impact of a age-related clonal hematopoiesis associated somatic mutation on monocyte-derived microglia and macrophages in the CNS, we took advantage of a mouse model that harbors a replacement of the murin Dnmt3a gene with a cDNA cassette encoding the human DNMT3A R882H variant. To seed the CNS with monocyte-derived cells from hDNMT3A mut hematopoietic stem cells, we engrafted Cx3cr1-gfp mice with bone marrow of 10-month-old Vav-Cre: hDNMT3A fl/fl mice. After 4 months following irradiation, endogenous microglia and leptomeningeal macrophages, and engrafted cells were isolated from both mutation and wild type groups for bulk RNAseq analysis.

2024-12-02 | GSE282223 | GEO

Oligodendrocyte progenitor cells and macrophages/microglia produce glioma stem cell niche at the tumor border

Project description:Characterization of the tumor border microenvironment is critical for improving prognosis in patients with GBM. Here, we compared microRNA (miRNA) expression in samples from the tumor, tumor border, and peripheral region far from tumor mass by miRNA microarray. The top three of miRNAs showing higher expression in the tumor border were related to oligodendrocyte differentiation, and pathologically oligodendrocyte lineage cells were increased in the border, where numbers of macrophages and microglia also colocalized. Medium cultured with oligodendrocyte progenitor cells (OPCs) and macrophages induced stemness and chemo-radioresistance in GBM cells. Thus, OPCs and macrophages/microglia may form a glioma stem cell niche at the tumor border, representing a novel promising target for prevention of recurrence.

2018-01-26 | GSE109628 | GEO

A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

Project description:A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

| PRJNA878792 | ENA

Gene expression profile of sorted microglia and CD206 border-associated macrophages obtained from mice

Project description:Gene expression profile of sorted microglia and CD206 border-associated macrophages obtained from mice

| PRJNA1109829 | ENA

Genome-Wide Expression Profiling of human tumor-infiltrating microglia/macrophages

Project description:Microglia isolated from glioma patients gain anti-tumor activities upon poly (I:C) stimulation. Expression profiles of human tumor-infiltrating microglia/macrophages before (untreated) and after treatment with poly (I:C) for 48h (induced). Tumor-infiltrating microglia/macrophages were isolated from freshly excised brain tumors

2011-12-31 | E-GEOD-25289 | biostudies-arrayexpress

Oligodendrocyte progenitor cells and macrophages/microglia produce glioma stem cell niche at the tumor border

Project description:Oligodendrocyte progenitor cells and macrophages/microglia produce glioma stem cell niche at the tumor border

| PRJNA431551 | ENA

Parenchymal border macrophages regulate CSF flow dynamics

Project description:Parenchymal border macrophages regulate CSF flow dynamics

| PRJNA778201 | ENA

A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

Project description:Genetic tools to target microglia specifically and efficiently from the early stages of the embryonic development are missing. Here we present Crybb1-Cre, a new constitutive Cre deleter producing a nearly complete recombination of embryonic brain macrophages (microglia and embryonic BAMs) by the perinatal period, with limited recombination leakage in peripheral myeloid cells. Using this tool, in combination with Flt3-Cre lineage tracer, scRNA-seq analysis and confocal imaging we were able to accurately fate-map embryonic derived versus monocyte derived BAMs in the mouse cortex and identified specific surface markers to resolve either population. Furthermore, we used Crybb1-Cre to delete the transcription factor SMAD4. Using multiomics analysis combining single-cell RNA-seq and ATAC-seq we showed that SMAD4-deficient microglia underwent an arrest of their homeostatic maturation and at the same time acquired a BAMs specification signature. By contrast, BAMs development was unaffected. Therefore, SMAD4 drives a transcriptional and epigenetic program that is indispensable for the commitment of brain macrophages to the microglia fate. This data provides a valuable resource to study molecular underpinnings of microglia development.

2023-02-02 | GSE213020 | GEO

iPSC-derived microglia carrying the TREM2 R47H/+ mutation are pro-inflammatory and promote synapse loss.

Project description:Genetic findings have highlighted key roles for microglia in the pathology of neurodegenerative conditions such as Alzheimer’s disease (AD). A number of mutations in the microglial protein TREM2 (triggering receptor expressed on myeloid cells 2) have been associated with increased risk for developing Alzheimer’s disease (AD), most notably the R47H/+ substitution. We employed gene editing and stem cell models to gain insight into the effects of the TREM2 R47H/+ mutation on human iPSC-derived microglia. We found transcriptional changes affecting numerous cellular processes, with R47H/+ cells exhibiting a pro-inflammatory gene expression signature. TREM2 R47H/+ also caused impairments in microglial movement and the uptake of multiple substrates, as well as rendering microglia hyper-responsive to inflammatory stimuli. We developed an in vitro laser-induced injury model in neuron-microglia co-cultures, finding an impaired injury response by TREM2 R47H/+ microglia. Furthermore, mouse brains transplanted with TREM2 R47H/+ microglia exhibited reduced synaptic density, with upregulation of multiple complement cascade components in TREM2 R47H/+ microglia suggesting inappropriate synaptic pruning as one potential mechanism. These findings identify a number of potentially detrimental effects of the TREM2 R47H/+ mutation on microglial gene expression and function likely to underlie its association with AD.

2024-03-06 | GSE241858 | GEO

iPSC-derived microglia carrying the TREM2 R47H/+ mutation are pro-inflammatory and promote synapse loss.

Project description:iPSC-derived microglia carrying the TREM2 R47H/+ mutation are pro-inflammatory and promote synapse loss.

| PRJNA1010350 | ENA