Microglia care for neurons through tunneling nanotubes [Dataset 2 Microglia mRNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE209971 | GEO | 2023/12/01
REPOSITORIES: GEO
Similar Datasets
Project description:We report the transfer of alpha-s-ynuclein aggregates from neurons to microglia and examined transcriptomic changes following protein extraction. By obtaining RNA samples, we performed differential expression analysis and generated gene ontology enrichment and network analysis.
2023-12-01 | GSE209970 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-12-01 | GSE209972 | GEO
Project description:We report the exchange of alpha-synuclein aggregates from one cell to another and examined transcriptomic changes following protein exchange. By obtaining 12,461 genes from isolated RNA samples, we performed differential expression analysis and generated gene ontology enrichment and network analysis. Differential expression (DE) analysis comparing alpha-synuclein-treated with untreated microglia identified 687 upregulated and 1502 downregulated genes. Upregulated genes were linked to inflammation, apoptosis, ER stress and intracellular protein targeting, while downregulated genes included categories related to mitosis, cytoskeleton and vesicle mediated transport. Co-culturing alpha-synuclein treated with untreated microglia largely suppressed the inflammatory and apoptotic phenotype of microglia thereby rescuing cells from cell death.
2021-09-28 | GSE152100 | GEO
Project description:Background: Cell-to-cell propagation of α-synuclein (α-syn) aggregates is thought to contribute to the pathogenesis of Parkinson’s disease (PD) and underlie the spread of α-syn neuropathology. Increased pro-inflammatory cytokine levels and activated microglia are present in PD and activated microglia can promote α-syn aggregation. However, it is unclear how microglia influence α-syn cell-to-cell transfer. Methods: We developed a clinically relevant mouse model to monitor α-syn prion-like propagation between cells; we transplanted wild-type mouse embryonic midbrain neurons into a mouse striatum overexpressing human α-syn (huα-syn) following adeno-associated viral injection into the substantia nigra. In this system, we depleted or activated microglial cells and determined the effects on the transfer of huα-syn from host nigrostriatal neurons into the implanted dopaminergic neurons, using the presence of huα-syn within the grafted cells as a readout. Results: First, we compared α-syn cell-to-cell transfer between host mice with a normal number of microglia to mice in which we had pharmacologically ablated 80% of the microglia from the grafted striatum. With fewer host microglia, we observed increased accumulation of huα-syn in grafted dopaminergic neurons. Second, we assessed the transfer of α-syn into grafted neurons in the context of microglia activated by one of two stimuli, lipopolysaccharide (LPS) or interleukin-4 (IL-4). LPS exposure led to a strong activation of microglial cells (as determined by microglia morphology and cytokine production) and significantly higher amounts of huα-syn in grafted neurons. In contrast, injection of IL-4 did not change the proportion of grafted dopamine neurons that contained huα-syn relative to controls. RNA sequencing analysis revealed differential gene expression between LPS and IL-4 injected mice; many genes were upregulated in LPS including those involved with the inflammatory response. Conclusions: The absence or the hyperstimulation of microglia affected α-syn transfer in the brain. Our results suggest that under resting, non-inflammatory conditions, microglia modulate the transfer of α-syn. Pharmacological regulation of neuroinflammation could represent a future avenue for limiting the spread of PD neuropathology.
2019-08-12 | GSE130683 | GEO
Project description:Intercellular communication within the bone marrow niche significantly influences leukemogenesis and the sensitivity of leukemic cells to therapy. However, the landscape of possible cell-cell interactions is still incomplete. Tunneling nanotubes (TNTs) are a novel mode of intercellular cross-talk. They are long, thin membranous conduits that enable the direct transfer of various cargo between cells. The present study found that TNTs are formed between leukemic and bone marrow stromal cells. Confocal three-dimensional reconstructions, correlative light-electron microscopy, and electron tomography provided evidence that TNTs transfer cellular vesicles between cells. The quantitative analysis demonstrated the stimulation of TNT-mediated vesicle transfer from stromal cells to leukemic cells by the stromal component. The vesicular cargo that was received from stroma cells conferred resistance to anti-leukemic treatment. Moreover, specific sets of proteins with a potential role in survival and the drug response were transferred within these vesicles. Altogether, we found that TNTs are involved in a novel and potent mechanism that participates in leukemia-stroma cross-talk and the stroma-mediated cytoprotection of leukemic cells. Our findings implicate TNT connections as a possible target for therapeutic interventions within the leukemia microenvironment to attenuate stroma-conferred protection.
2022-02-16 | PXD011013 | Pride
Project description:Intercellular communication within the bone marrow niche significantly influences leukemogenesis and the sensitivity of leukemic cells to therapy. However, the landscape of possible cell-cell interactions is still incomplete. Tunneling nanotubes (TNTs) are a novel mode of intercellular cross-talk. They are long, thin membranous conduits that enable the direct transfer of various cargo between cells. The present study found that TNTs are formed between leukemic and bone marrow stromal cells. Confocal three-dimensional reconstructions, correlative light-electron microscopy, and electron tomography provided evidence that TNTs transfer cellular vesicles between cells. The quantitative analysis demonstrated the stimulation of TNT-mediated vesicle transfer from stromal cells to leukemic cells by the stromal component. The vesicular cargo that was received from stroma cells conferred resistance to anti-leukemic treatment. Moreover, specific sets of proteins with a potential role in survival and the drug response were transferred within these vesicles. Altogether, we found that TNTs are involved in a novel and potent mechanism that participates in leukemia-stroma cross-talk and the stroma-mediated cytoprotection of leukemic cells. Our findings implicate TNT connections as a possible target for therapeutic interventions within the leukemia microenvironment to attenuate stroma-conferred protection.
2019-11-11 | PXD013504 | Pride
Project description:To detect total RNA in microglia derived from AD mice (5xFAD) brain we single cell sorted Cd11b+ and Cd45+ cells divided by Methoxy-X04 staining (Ab aggregates) positivity We performed differentially expression analysis of RNA-seq of wild-type microglia (Me-X04 neg), non-phagocytic AD microglia (Me-X04 neg), phagocytic AD microglia (Me-X04 positive)
2024-03-20 | GSE229418 | GEO
Project description:To detect miRNAs in microglia derived from AD mice (5xFAD) brain we single cell sorted Cd11b+ and Cd45+ cells divided by Methoxy-X04 staining (Ab aggregates) positivity We performed differentially expression analysis of RNA-seq of wild-type microglia (Me-X04 neg), non-phagocytic AD microglia (Me-X04 neg), phagocytic AD microglia (Me-X04 positive)
2024-03-20 | GSE229417 | GEO
Project description:Using Illumina MouseWG-6v2 microarrays, we investigated the gene transcription changes in microglia and peripheral monocytes after contextual fear conditioning of C57BL/6J mice. Mice were trained with or without a single minimized footshock stimulation (0-s or 2-s, 0.4 mA) and re-exposed to the training context without footshock for three different durations 24 h later: 0 min (FS0), 3 min (FS3), or 30 min (FS30). Whole brain microglia and peripheral monocytes were prepared 24 h after re-exposure using a neural tissue dissociation kit, including non-footshock controls for two re-exposure durations (Con3 and Con30). The data can be valuable for researchers interested in glial cells and neurotransmission studies and are related to the research article “Contextual fear conditioning regulates synapse-related gene transcription in mouse microglia”.
2022-10-28 | E-MTAB-12361 | biostudies-arrayexpress
Project description:Determination of the mechanism by which microglia regulate growth of brain tumor initiating cells (BTICs) and differentiation. Results identify the factors involved in the regulation and provide mechanistic basis. We subjected brain tumor initiating cells to microarray to determine the genes involved in BTICs growth and differentiation when exposed to microglia conditioned medium (MCM) for 6h. BTICs were grown in MCM or control medium for 6h, and media was removed and then the cells were subjected for RNA extraction and hybridization on Affymatrix microarrays. Three (3) control and four (4) MCM samples were generated. The overall objective was to collect the RNA from the MCM exposed differentiated BTICs.
2013-11-06 | E-GEOD-52127 | biostudies-arrayexpress