Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microglia-derived Il6 deficient Vs floxed mice with/without cryolesion

ABSTRACT: Microglia-derived Il6 deficient Vs floxed mice with/without cryolesion

PROVIDER: PRJNA575751 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Microglia-derived Il6 deficient Vs floxed mice with/without cryolesion

Project description:We have examined the role of microglia-derived IL-6 by analyzing the transcriptome of the brain cortex following a cryolesion. We performed oligonucleotide array analysis using the right fronto-parietal cortex of microglia-derived Il6 deficient (Il6ΔMic) and floxed (Il6lox/lox) mice , under control and cryolesion conditions.

2020-10-03 | GSE138410 | GEO

MDMs Solvent, AA, IL6, AA+IL6

Project description:MDMs Solvent, AA, IL6, AA+IL6

| PRJEB36942 | ENA

Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:CX3CR1, one of the highest expressed genes in microglia in mice and humans, is implicated in numerous microglial functions. However, the molecular mechanisms underlying Cx3cr1 signaling are not well understood. Here, we analyzed transcriptomes of Cx3cr1-deficient microglia under varying conditions by RNA-Seq. In 2 mos mice, Cx3cr1 deletion resulted in the downregulation of a subset of immune-related genes, without substantial epigenetic changes in markers of active chromatin. Surprisingly, Cx3cr1-deficient microglia from young mice exhibited a transcriptome consistent with that of aged Cx3cr1-sufficient animals, suggesting a premature aging transcriptomic signature. Immunohistochemical analysis of microglia in young and aged mice revealed that loss of Cx3cr1 modulates microglial morphology in a compatible fashion. Our results suggest that CX3CR1 may regulate microglial function in part by modulating the expression levels of a subset of inflammatory genes during chronological aging, making Cx3cr1-deficient mice useful for studying aged microglia.

2019-10-01 | GSE130960 | GEO

In vivo response of microglia to Aβ and prostaglandin-E2 EP2 receptor signaling

Project description:Microglia, the innate immune cells of the central nervous system, perform critical inflammatory and non-inflammatory functions to maintain homeostasis and normal neural function. However in Alzheimer’s disease (AD), these beneficial functions become progressively impaired, contributing to synapse and neuron loss and cognitive impairment. The inflammatory cyclooxygenase-PGE2 pathway, including the PGE2 receptor EP2, is implicated in AD development, both in human epidemiology and in transgenic models of AD. To test the transcriptional responses of EP2-deficient microglia to Aβ in vivo, we used mice in which the EP2 receptor is conditionally deleted in microglia using the CD11b-Cre transgene and floxed alleles of the EP2 gene. By injecting these mice with Aβ ICV and isolating microglia from the brains, we have been able to establish the transcriptional response of microglia to Aβ in vivo and test how EP2 deletion in microglia affects this response. 8 month-old C57BL/6 mice, of the genotype CD11b-Cre; EP2+/+ or CD11b-Cre; EP2lox/lox, were injected I.C.V. with either Aβ or vehicle. 48 hours after injection, the mice were sacrificed and transcardially perfused with cold heparinized 0.9% NaCl. Brains were then removed from the mice and pooled, two brains of the same genotype per sample, to ensure adequate cell and RNA yield. The brains were then enzymatically dissociated for microglia isolation using the Neural Tissue Dissociation Kit (P), MACS Separation Columns (LS), and magnetic CD11b Microbeads from Miltenyi Biotec according to the manufacturer's protocol. Immediately after isolating the microglia, RNA was extracted from the cells for microarray analysis.

2015-02-20 | E-GEOD-57181 | biostudies-arrayexpress

Cx3cr1-deficient microglia exhibit a premature aging transcriptome

2019-11-25 | GSE131869 | GEO

Proteomics of CLN3-deficient murine microglia identifies a disease associated phenotype with lysosomal alterations

Project description:Loss-of-function mutations in CLN3 cause juvenile Batten disease, featuring neurodegeneration and early-stage neuroinflammation. How loss of CLN3 function leads to early neuroinflammation is not yet understood. Here, we have comprehensively studied microglia from Cln3∆ex7/8 mice, a genetically accurate disease model. Loss of CLN3 function in microglia leads to lysosomal storage material accumulation and abnormal morphology of subcellular organelles. We also discovered pathological proteomic signatures consistent with defects in lysosomal function and indicative of abnormal lipid metabolism. CLN3-deficient microglia were unable to efficiently turnover myelin and metabolize the associated lipids, showing defects in lipid droplet formation and cholesterol accumulation.

2024-10-23 | PXD048550 | Pride

Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:Cx3cr1-deficient microglia exhibit a premature aging transcriptome

| PRJNA542087 | ENA

ChIP-sequencing of PRMT1 proficient and deficient microglia

Project description:ChIP-sequencing of PRMT1 proficient and deficient microglia

| PRJNA844360 | ENA

RNA-sequencing of QKI proficient and deficient microglia

Project description:RNA-sequencing of QKI proficient and deficient microglia

| PRJNA656802 | ENA

RNA-sequencing of PRMT1 proficient and deficient microglia

Project description:RNA-sequencing of PRMT1 proficient and deficient microglia