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Prevention of MECP2 phosphorylation at S423 changes global transcription in primary cortical neurons co-cultured with BV2 cells upon LPS/IFNγ-induced activation.

ABSTRACT: Prevention of MECP2 phosphorylation at S423 changes global transcription in primary cortical neurons co-cultured with BV2 cells upon LPS/IFNγ-induced activation.

PROVIDER: PRJNA701569 | ENA |

REPOSITORIES: ENA

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Prevention of MECP2 phosphorylation at S423 changes global transcription in primary cortical neurons co-cultured with BV2 cells upon LPS/IFNγ-induced activation.

Project description:Methyl-CpG-binding protein 2 (MECP2) is a transcriptional regulator critical for synaptic function. Dysfunction of synapses, in turn, as well as microglia-mediated neuroinflammation belong to the earliest pathological events in Alzheimer’s disease (AD). Functional versatility of MECP2, including its affinity for different binding partners, transcriptional regulation of different gene sets, and effects on neuronal plasticity, are modulated by post-translational modifications, such as phosphorylation. To characterize expression changes through blocking of MECP2 S80 and S423 phosphorylation in neuron-BV2 co-cultures upon induction of neuroinflammation, mouse primary cortical neurons were transduced with MECP2-WT and MECP2-S80A and MECP2-S423A phopsho-variants. Neuroinflammation was induced with LPS/IFNγ and the samples were subjected to RNA sequencing. In neurons co-cultured with BV2 cells, blocking of MECP2 S423 phosphorylation increased the expression of several genes important for neuron and synapse maintenance and protection upon inflammatory stress conditions. Blocking of S80 phosphorylation did not lead to major global expression changes.The results suggest that MECP2 S423 phosphorylation might play a role in activation of neuronal gene expression conveying neuroprotection under neuroinflammation related stress conditions.

2021-02-13 | GSE166670 | GEO

RNA-seq analysis of murine microglial BV2 cells treated with interferon-gamma (IFNγ)

Project description:BV2 cells were treated with IFNγ. Wildtype cells were compared to cells made deficient for Atg5 via CRISPR/Cas9.

2020-06-12 | GSE132739 | GEO

LPS and Telmisartan co-treatment of microglial BV2 cells

Project description:LPS and Telmisartan co-treatment of microglial BV2 cells.

2018-07-02 | GSE108669 | GEO

LPS, Telmisartan and GW9662 co-treatment of microglial BV2 cells

Project description:LPS, Telmisartan and GW9662 co-treatment of microglial BV2 cells.

2018-07-02 | GSE108670 | GEO

RNA-seq analysis of murine microglial BV2 cells treated with interferon-gamma (IFNγ)

Project description:RNA-seq analysis of murine microglial BV2 cells treated with interferon-gamma (IFNγ)

| PRJNA548876 | ENA

Transcriptome analysis of BV2 cells in response to LPS stimulation

Project description:Mouse microglia (BV2 cells) were stimulated with a TLR4 ligand (E. coli LPS, 1 µg/ml) for 4h. The Agilent SurePrint G3 Mouse Gene Expression Microarray (G4852A) was used for the analysis, which provides full coverage of genes and transcripts with the most up-to-date content, including mRNAs and lincRNAs (http://www.chem.agilent.com/store/en_US/Prod-G4852A/G4852A). BV2 cells were grown to 80% confluence for four groups: the siRNA control (Group A, cells treated with a non-specific scrambied siRNA control), the LPS-stimulated (Group B, cells treated with the siRNA control plus LPS stimulation), lincRNA-Cox2 siRNA (Group C, cells treated with an siRNA to lincRNA-Cox2), and lincRNA-Cox2 siRNA/LPS stimulated (Group D, cells treated with the lincNRA-Cox2 siRNA plus LPS stimulation). Cells were treated with the siRNAs for 24h, followed by additional culture for 4h in the presence or absence of LPS (E. coli LPS, 1 µg/ml). Total RNAs were prepared with the RNeasy Mini kit (Qiagen) according to the manufacturer’s instruction (Ambion).

2016-04-18 | E-MTAB-3450 | biostudies-arrayexpress

RNA-seq of M-CSF differentiated human peripheral monocyte-derived macrophages (MDMs) activated with short exposure (3hours) to LPS, or long exposure (24 hours) to LPS, LPS with IFNγ, IFNγ, IL-4, IL-10, and dexamethasone

Project description:The goal of this experiment was to validate a classification model built on other bulk transcriptomic data that was capable of identifying in vitro stimulated M-CSF differentiated macrophages. Specifically, the classification model was capable of distinguishing: M-LPSearly (2-4 hours) M-LPSlate (18-24 hours) M-LPS+IFNγ M-IFNγ M-IL4 M-IL-10 M-dex

2020-01-06 | E-MTAB-7572 | biostudies-arrayexpress

Exosomal-miRNA sequencing of optineurin gene knockdown BV2 cells and wild type BV2 cells

Project description:To compare the miRNA profiles in exosomes derived from optineurin gene knockdown (Optn-KD)BV2s cells and wild type (WT) BV2 cells, BV2 cells were divided into two groups, Optn-KD group or WT group. We treated the Optn-KD group with Optn siRNA for 24 hours. Then, MiRNA profiles for each group were examined by Illumina HiSeq4000. We found differentiated miRNA profiles in the two groups. Compared with WT BV2 cell-derived exosomes, 4 miRNAs (miR-125b-5p, miR-351-5p, miR-505-5p, miR-novel-chr8_37700) were up-regulated and 2 miRNAs (miR-574-5p, miR-99b-5p) were down-regulated in Optn-KD BV2 cell-derived exosomes. This study provides a framework for characterizing the exosomal-miRNAs in Optn-KD BV2 cells.

2021-03-19 | GSE169175 | GEO

Gene expression profiles in BV2 cells with or without PGC-1α overexpression after LPS stimulation

Project description:PGC-1α overexpression in microglia protects against ischemia-induced brain damage in mice. To investigate the underlying mechanism of PGC-1α in vitro, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes with the potential to change the BV2 cells function. Indeed, PGC-1α overexpression alters the gene expression profiles of BV2 cells, this revealed that PGC-1α could inhibit the production of IL-1β and pro-inflammatory cytokines.

2020-06-19 | GSE152769 | GEO

MeCP2 heterochromatin organization is modulated by arginine methylation and serine phosphorylation

Project description:Rett syndrome is a human intellectual disability disorder that is associated with mutations in the X-linked MECP2 gene. Theepigenetic reader MeCP2 binds to methylated cytosines on the DNA and regulates chromatin organization. We have shownpreviously that MECP2 Rett syndrome missense mutations are impaired in chromatin binding and heterochromatinreorganization. Here, we performed a proteomics analysis of post-translational modifications of MeCP2 isolated from adult mousebrain. We show that MeCP2 carries various post-translational modifications, among them phosphorylation on S80 and S421, whichlead to minor changes in either heterochromatin binding kinetics or clustering. We found that MeCP2 is (di)methylated on severalarginines and that this modification alters heterochromatin organization. Interestingly, we identified the Rett syndrome mutationsite R106 as a dimethylation site. In addition, co-expression of protein arginine methyltransferases 1 and 6 lead to a decrease ofheterochromatin clustering. Altogether, we identified and validated novel modifications of MeCP2 in the brain and show that thesecan modulate its ability to bind as well as reorganize heterochromatin, which may play a role in the pathology of Rett syndrome.

2022-10-15 | PXD033696 | Pride

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