<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Owen Robert Dando</submitter><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><organism>Mus musculus</organism><species>Mus musculus</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-14572</full_dataset_link><description>Nrf2 is a potential therapeutic target for various neurological disorders including neurodegenerative diseases, but the mechanisms behind Nrf2-mediated cytoprotection are incompletely understood. While an anti-inflammatory effect is a popular hypothesis, Nrf2 is highly expressed in microglia, astrocytes and brain endothelial cells in the adult brain, and the brain cell type-specific role of Nrf2 in regulating the basal transcriptome and controlling neuroinflammation is unknown. To address this, we employed three inducible conditional Nrf2 knockout mice in which Nrf2 is deleted in microglia, astrocytes, and brain endothelial cells respectively, in a model of system inflammatory challenge.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Library Construction - RNA-seq libraries were prepared by Edinburgh Genomics using the Illumina TruSeq stranded mRNA-seq kit, according to the manufacturer’s protocol (Illumina).</sample_protocol><sample_protocol>Sample Collection - Single brain cells were isolated using Adult Brain Dissociation kit (Miltenyie, 130-107-677, Germany) as per the manufacturer’s instructions. The single brain cell suspension was then incubated with antibodies against CD31 (Biolegend, 102523, UK) CD11b (Biolegend, 101205, UK), ACSA2 (Miltenyie, 130-116-245, Germany), O4 (Miltenyie, 130-117-357, Germany), CD45 (Biolegend, 103125, Germany) for 15 minutes in ice, washed with PBS and then immediately FACS sorted into RNAprotect Cell Reagent (Qiagen, 76526, UK) under the gates of CD31+CD45-ACSA2- for brain endothelial cells, LY6G-CD11b+CD45low for microglia, ACSA+O4- for astrocytes.</sample_protocol><sample_protocol>Nucleic Acid Extraction - RNA extraction was carried out using the RNeasy Plus Micro Kit (Qiagen) as per the manufacturer’s instructions.</sample_protocol><sample_protocol>Sequencing - Libraries were sequenced on an Illumina NovaSeq 6000.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><pubmed_authors>Owen Robert Dando</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNA-seq of endothelial cells, astrocytes and microglia in cell-type specific Nrf2 knockout mice, in a model of system inflammation</name><description>Nrf2 is a potential therapeutic target for various neurological disorders including neurodegenerative diseases, but the mechanisms behind Nrf2-mediated cytoprotection are incompletely understood. While an anti-inflammatory effect is a popular hypothesis, Nrf2 is highly expressed in microglia, astrocytes and brain endothelial cells in the adult brain, and the brain cell type-specific role of Nrf2 in regulating the basal transcriptome and controlling neuroinflammation is unknown. To address this, we employed three inducible conditional Nrf2 knockout mice in which Nrf2 is deleted in microglia, astrocytes, and brain endothelial cells respectively, in a model of system inflammatory challenge.</description><dates><release>2025-07-15T00:00:00Z</release><modification>2025-07-15T09:01:11.724Z</modification><creation>2024-10-31T22:28:52.062Z</creation></dates><accession>E-MTAB-14572</accession><cross_references><ENA>ERP165682</ENA><Biostudies>E-MTAB-14404</Biostudies><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>