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Expression data from microglial cell line BV-2

ABSTRACT: Expression data from microglial cell line BV-2

PROVIDER: PRJNA606033 | ENA |

REPOSITORIES: ENA

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Expression data from microglial cell line BV-2

Project description:Microglial morphology is tightly associated with aspects of their functions during the postnatal stage. It is affected by not only intrinsic cues but also external factors. To pursue the novel factor that controls microglial morphology, we conducted microarray analysis using microglial cell line BV-2. We identified distinct candidates of both up-regulated and down-regulated genes from this experiment.

2020-02-12 | GSE145098 | GEO

Genome-wide identification and analysis of gene expression in BV-2, a murine microglial cell line, infected with rabies virus CVS-11 (Challenge virus standard)

Project description:The hypothesis tested in the present study was that rabies virus (RABV) infection affects the gene expression in microglial cells. Results provide important information that RABV infection led to alteration of gene expression in microglia. A twelve-chip study was performed using total RNA isolated from RABV- or mock-infected BV-2 at 12, 24, or 48 hpi.

2014-10-10 | E-GEOD-35684 | biostudies-arrayexpress

Transcriptome analysis of BV-2 microglial cells displaying a CRISPR/Cas9-induced knockout of peroxisomal genes (Abcd1, Abcd2, Abcd1/Abcd2, Acox1)

Project description:Here, we report the characterization and the comparison of the transcriptomes of BV-2 murine microglial mutant cell lines (CRISPR/Cas9-edited mutations in peroxisomal genes) by RNA-sequencing. Microglia is suspected to play a major role in the neurodegenerative processes observed in peroxisomal leukodystrophies. From CRISPR/Cas9-edited BV-2 microglial cell lines, we aimed at exploring the transcriptomic consequences of a defect of peroxisomal beta-oxidation.

2023-03-28 | GSE200022 | GEO

Transcriptome analysis of the LPS response of BV-2 microglial cells displaying a CRISPR/Cas9-induced knockout of peroxisomal genes (Abcd1/Abcd2 or Acox1)

Project description:In X-linked adrenoleukodystrophy (X-ALD), the most common peroxisomal disorder, microglial defect is suggested to prime and amplify the neuroinflammatory process. By using CRISPR/Cas9 gene editing, we recently established BV-2 microglial cell models to study the impact of dysfunctional peroxisomal b-oxidation and demonstrated the emergence of a disease-associated microglial signature in these cell lines. Their transcriptomic analysis suggested consequences on immune response. To go further, we have used RNA-sequencing and functional assays related to immune response to compare the WT and mutant BV-2 cell lines in basal conditions or upon lipopolysaccharide (LPS) stimulation.

2024-01-01 | GSE237635 | GEO

Docosahexaenoic acid attenuates metabolic dysfunctions induced by lipopolysaccharide in BV-2 microglial cells

Project description:Microglial cell activation has been linked to many neurodegenerative diseases. Upon stimulation by lipopolysaccharide (LPS), a number of proteins involved in inflammatory and oxidative pathways are activated. Production of nitric oxide has been regarded as a signature marker of inflammatory responses. Our recent studies demonstrated the effects of docosahexaenoic acid (DHA) to inhibit the LPS-induced inflammatory responses in BV-2 microglial cells. DHA also can upregulate the anti-oxidative pathway involving nuclear factor erythroid 2-Like 2 (Nrf2) and synthesis of heme oxygenase-1 (HO-1), a potent anti-oxidative enzyme. In order to further understand the proteins involved, this study used a label-free quantitative proteomics approach to examine effects of DHA and LPS on proteins and signaling pathways in microglial cells.

2020-04-20 | PXD013086 | Pride

Microarray and Pathway Analysis Reveal Distinct Mechanisms Underlying Cannabinoid-Mediated Modulation of LPS-Induced Activation of BV-2 Microglial Cells

Project description:Cannabinoids are known to exert immunosuppressive activities. However, the mechanisms which contribute to these effects are unknown. Using lipopolysaccharide (LPS) to activate BV-2 microglial cells, we examined how Δ9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, and cannabidiol (CBD) the non-psychoactive component, modulate the inflammatory response. Microarray analysis of genome-wide mRNA levels was performed using Illumina platform and the resulting expression patterns analyzed using the Ingenuity Pathway Analysis to identify functional subsets of genes, and the Ingenuity System Database to denote the gene networks regulated by CBD and THC.

2015-07-09 | E-GEOD-70689 | biostudies-arrayexpress

Microarray and Pathway Analysis Reveal Distinct Mechanisms Underlying Cannabinoid-Mediated Modulation of LPS-Induced Activation of BV-2 Microglial Cells

2015-07-09 | GSE70689 | GEO

RNA Sequencing Facilitates Quantitative Analysis of BV-2 Transcriptomes

Project description:Using RNA-seq, we report here that BV-2 microglial cells have a distinct transcriptomic signature and express a unique cluster of transcripts in response to 4 hrs LPS.

2016-12-04 | GSE75714 | GEO

Genome-wide expression analysis of memory-like inflammatory responses in murine micoglial cells (BV-2 immortalized microglial cell line)

Project description:Genome-wide expression analysis of memory-like inflammatory responses in murine micoglial cells (BV-2 immortalized microglial cell line)

| PRJNA566425 | ENA

Microarray analysis to evaluate the role of USP18 in primary microglia and the microglia cell line BV-2

Project description:Microglia are tissue macrophages of the central nervous system (CNS) that control tissue homeostasis, and as such they are crucially important for organ integrity. Microglia dysregulation is thought to be causal for a group of neuropsychiatric, neurodegenerative and neuroinflammatory diseases, called ‘microgliopathies’. However, how the intracellular stimulation machinery in microglia is controlled is poorly understood. By using expression studies, we identified the ubiquitin-specific protease (Usp) 18 in white matter microglia that essentially contributes to microglial quiescence under homeostatic conditions. We further found that microglial Usp18 negatively regulated the activation of STAT1 and concomitant induction of interferon-induced genes thereby disabling the termination of IFN signalling. Unexpectedly, the Usp18-mediated feedback loop was independent from the catalytic domain of the protease but instead required the interacting region of Ifnar2. Additionally, the absence of Ifnar1 completely rescued microglial activation indicating a tonic IFN signal mediated by receptor interactions under non-diseased conditions. Finally, conditional depletion of Usp18 only in myeloid cells significantly enhanced the disease burden in a mouse model of CNS autoimmunity, increased axonal and myelin damage and determined the spatial distributions of CNS lesions that shared the same STAT1 signature as myeloid cells found in active multiple sclerosis (MS) lesions. These results identify Usp18 as novel negative regulator of microglia activation, demonstrate a protective role of the IFNAR pathway for microglia and establish Usp18 as potential therapeutic target for the treatment of MS. Primary microglia (WT, USP18ko and USP18_C61A mice) and BV-2 cells (treated with control siRNA or siRNA against USP18) were incubated with 500 U/ml IFN-b. At different timepoints (0h, 6h, and 24h) RNA samples were taken and analyzed via Microarray

2015-04-20 | E-GEOD-61500 | biostudies-arrayexpress

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