Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq analysis of primary astrocyte and microglia under Aβ40WT and Aβ42WT fibrils treatment

ABSTRACT: To investigate the influence of Aβ40WT and Aβ42WT fibrils on astrocyte and microglia, we isolated astrocyte and microglia from P2 SD rats and treated glia cells with Aβ40WT and Aβ42WT fibrils for 24 hours. We then performed gene expression profiling analysis using data obtained from RNA-seq of astrocyte and microglia treated with Aβ fibrils.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE211198 | GEO | 2022/08/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Microglial Piezo1 senses Aβ fibrils stiffness to restrict Alzheimer’s disease

Project description:Microglial Piezo1 senses Aβ fibrils stiffness to restrict Alzheimer’s disease

| PRJNA818969 | ENA

Transcriptome analysis of LRRK2 knock-out microglia cells reveals T alterations of inflammatory- and oxidative stress-related pathways upon treatment with α-synuclein fibrils

Project description:We used the RNA-Sequencing to obtain transcriptomic profiles of LRRK2 wild-type (WT) and knock-out (KO) microglia cells treated with α-synuclein pre-formed fibrils (PFFs) or lipopolysaccharide (LPS) as a general inflammatory insult. Conclusion: overall, the results suggest that microglial LRRK2 may contribute to the pathogenesis of PD via altered oxidative stress signaling.

2021-10-26 | GSE186483 | GEO

TNFα and α-synuclein fibrils differently regulate human astrocyte immune reactivity and impair mitochondrial respiration

Project description:TNFα and α-synuclein fibrils differently regulate human astrocyte immune reactivity and impair mitochondrial respiration

| PRJNA701924 | ENA

Microglial Piezo1 senses Aβ fibrils stiffness to restrict Alzheimer’s disease

Project description:Alzheimer's disease (AD) is associated with the formation of extracellular amyloid-β (Aβ) plaque, perturbing the mechanical properties of brain tissue. Microglia sense and integrate biochemical and mechanical cues in their local microenvironment, intimately linked with AD progress. However, little is known about how microglial mechanosensing pathways are implicated in AD pathogenesis. Gene Ontology (GO) analysis of the significantly down-regulated genes in Piezo1 conditional knockout microglia revealed a significant functional reduction in synapse organization, cell-substrate adhesion, and cytoskeleton system-based events (morphogenesis, migration, and endocytosis) in 5×FAD mice.

2022-03-26 | GSE199217 | 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

Astrocyte-microglia interaction drives Aβ induced initial memory deficit

Project description:Based on behavioral paradigms, olfactory memory impaiment was considered as the first congnitive decline symptom in 5xFAD mice at 4-month-old. Proteomes in olfactory memory associated brain region, piriform cortex, at different stages were analyzed. The results indiciated that proteins alterations at different stages are diverse, but the core regulatory network involved in AD pathogenesis is conservd. Microglia and astrocyte specific proteins are enriched in the networks and associated with glial cell activation in the initial cognitive impairment stage. It implied the mutual effect of the two glial cells plays an essential role in Aβ induced initial AD pathogenesis.

2023-03-13 | PXD040802 | iProX

Design, characterization, and use of a novel amyloid β-protein control for assembly, neurotoxicity, and gene expression studies

Project description:A key pathogenic agent in Alzheimer’s disease (AD) is the amyloid β-protein (Aβ), which self-assembles into a variety of neurotoxic structures. Establishing structure-activity relationships for these assemblies is critical for proper therapeutic target identification and design. We examined the effects of Aβ monomers, dimers, higher-order oligomers, and fibrils on gene expression in primary rat hippocampal neurons. As opposed to “reverse” Aβ or non-Aβ peptides typically used as controls in such studies, we designed novel scrambled Aβ peptides predicted to behave distinctly from native Aβ. Significant changes in gene expression were observed for all peptide assemblies, but fibrils induced the largest changes. Significant changes in gene expression were observed for all peptide assemblies, but fibrils induced the largest changes. Weighted gene co-expression network analysis (WGCNA) revealed two predominant gene modules related to Aβ treatment. Many genes within these modules were associated with inflammatory signaling pathways

2016-08-24 | GSE85952 | GEO

Astrocytic interleukin-3 programs microglia and limits Alzheimer’s disease

Project description:Communication within the glial cell ecosystem is essential for neuronal and brain health1–3. The influence of glial cells on the accumulation and clearance of β-amyloid (Aβ) and neurofibrillary tau in the brains of individuals with Alzheimer’s disease (AD) is poorly understood, despite growing awareness that these are therapeutically important interactions4,5. Here we show, in humans and mice, that astrocyte-sourced interleukin-3 (IL-3) programs microglia to ameliorate the pathology of AD. Upon recognition of Aβ deposits, microglia increase their expression of IL-3Rα—the specific receptor for IL-3 (also known as CD123)—making them responsive to IL-3. Astrocytes constitutively produce IL-3, which elicits transcriptional, morphological, and functional programming of microglia to endow them with an acute immune response program, enhanced motility, and the capacity to cluster and clear aggregates of Aβ and tau. These changes restrict AD pathology and cognitive decline. Our findings identify IL-3 as a key mediator of astrocyte–microglia cross-talk and a node for therapeutic intervention in AD.

2021-06-02 | GSE163289 | 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

Analysis of microglia responses following astrocyte knockdown of interferon gamma signaling during EAE.

Project description:We identify pathways in microglia regulated by astrocyte interferon gamma signaling during EAE

2021-01-09 | GSE154389 | GEO