Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of 8hr LPS-stimulated bone marrow-derived macrophages from wild type, Ch25h-deficient, and LXRab knockout mice

ABSTRACT: 25-hydroxycholesterol has been demonstrated to regulate SREBP processing, yet Ch25h-deficient mice have no cholesterol abnormalities. Using RNA-seq, we find that LPS-stimulated, Ch25h-deficient BMDMs have dysregulated SREBP target genes, demonstrating that 25-hydroxycholesterol is an induced repressor of SREBP during inflammatory settings. mRNA profiles from day 7 M-CSF bone marrow-derived macrophages (wild type, Ch25h-knockout, LXR-double knockout, were generated by deep sequencing on an Illumina HiSeq 2500. Sequence reads passing a quality filter were aligned to the mouse genome (mm10) using STAR.

ORGANISM(S): Mus musculus

SUBMITTER: Jason Cyster

PROVIDER: E-GEOD-58993 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Inflammation. 25-Hydroxycholesterol suppresses interleukin-1-driven inflammation downstream of type I interferon.

Reboldi Andrea A Dang Eric V EV McDonald Jeffrey G JG Liang Guosheng G Russell David W DW Cyster Jason G JG

Science (New York, N.Y.) 20140801 6197

Type I interferon (IFN) protects against viruses, yet it also has a poorly understood suppressive influence on inflammation. Here, we report that activated mouse macrophages lacking the IFN-stimulated gene cholesterol 25-hydroxylase (Ch25h) and that are unable to produce the oxysterol 25-hydroxycholesterol (25-HC) overproduce inflammatory interleukin-1 (IL-1) family cytokines. 25-HC acts by antagonizing sterol response element-binding protein (SREBP) processing to reduce Il1b transcription and t ...[more]

PMID: 25104388

Similar Datasets

RNA-seq of 8hr LPS-stimulated bone marrow-derived macrophages from wild type, Ch25h-deficient, and LXRab knockout mice

Project description:25-hydroxycholesterol has been demonstrated to regulate SREBP processing, yet Ch25h-deficient mice have no cholesterol abnormalities. Using RNA-seq, we find that LPS-stimulated, Ch25h-deficient BMDMs have dysregulated SREBP target genes, demonstrating that 25-hydroxycholesterol is an induced repressor of SREBP during inflammatory settings.

2014-08-08 | GSE58993 | GEO

The response to PAM3CSK4 (PAM3) of bone marrow derived macrophages treated with 25-hydroxycholesterol (RNA-Seq).

Project description:Bone marrow derived macrophages from C57BL/6 or Ch25h-/- mice (female) were treated with 25-hydroxycholesterol and then stimulated with PAM3CSK4.

2024-04-03 | GSE201129 | GEO

The response to lipopolysaccharide (LPS) of bone marrow derived macrophages treated with oxysterol binding protein (OSBP) inhibitors

Project description:Bone marrow derived macrophages from C57BL/6 or Ch25h-/- mice (female) were treated with 25-hydroxycholesterol, itraconazole, or Osw-1 and then stimulated with lipopolysaccharide.

2024-04-03 | GSE201128 | GEO

Transcription profiling of potent induction of flowering in A. thaliana by elevated temperature

Project description:Plants were grown on soil for 35 days under short day conditions (8hrs light/16hrs dark) at 16¡ÄC and 65% relative humidity. Flowering was induced by shifting either to long day conditions (16/8) at 16¡ÄC and 65% relative humidity or to 25¨¬C in short days (8/16). Samples were taken at day 0, 2, 5 and 9 after shifting.

2006-06-02 | E-MEXP-728 | biostudies-arrayexpress

LC-MSMS of primary AML class I immunopeptidome (ERE-derived MAPs identification approach)

Project description:The development of therapeutic anticancer vaccines calls for the identification of tumor-specific antigens (TSAs). Though a combination of four cutting-edge proteogenomic approaches, we performed a deep exploration of the MHC-I presented peptides (MAPs) of 19 acute myeloid leukemia (AML) patients and identified various TSAs that could serve for the design of an anti-AML vaccine.

2021-03-19 | PXD018542 | Pride

Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes [MG_U74Cv2]

Project description:The synthesis of fatty acids and cholesterol is regulated by three membrane-bound transcription factors: sterol regulatory element-binding proteins (SREBP)-1a, -1c, and -2. Their function in liver has been characterized in transgenic mice that overexpress each SREBP isoform and in mice that lack all three nuclear SREBPs because of gene knockout of SREBP cleavage-activating protein (SCAP) required for nuclear localization of SREBPs. Here, we use oligonucleotide arrays hybridized with RNA from livers of three lines of mice (transgenic for SREBP-1a, transgenic for SREBP-2, and knockout for SCAP) to identify genes that are likely to be direct targets of SREBPs in liver. Application of stringent combinatorial criteria to the transgenic/knockout approach allows identification of genes whose activities are likely controlled directly by the SREBPs.

2017-08-05 | GSE102258 | GEO

Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes [MG_U74Bv2]

2017-08-05 | GSE102257 | GEO

Combined analysis of oligonucleotide microarray data from transgenic and knockout mice identifies direct SREBP target genes [MG_U74Av2]

2017-08-05 | GSE102256 | GEO

Analysis of Wild Type and hepatocyte-specific CD36 knockout (CD36LKO) mice liver Transcriptomes under high fat diet (HFD)

Project description:We generated hepatocyte-specific CD36 knockout (CD36LKO) mice to study in vivo effects of CD36 on de novo lipogenesis (DNL) under high fat diet (HFD). Lipid deposition and DNL were analyzed in primary hepatocytes isolated from CD36LKO mice or HepG2 cells with CD36 overexpression. RNA-sequence, co-immunoprecipitation and proximity ligation assay were carried out to determine its role in regulating DNL. Results: Hepatic CD36 expression was upregulated in NAFLD mice and patients, and CD36LKO mice exhibited attenuated HFD-induced hepatic steatosis and insulin resistance. We identified hepatocyte CD36 as a key regulator for DNL in the liver. Sterol regulatory element-binding protein 1 (SREBP1) and its downstream lipogenic enzymes such as FASN, ACCα and ACLY were significantly downregulated in the liver of HFD-fed CD36LKO mice, whereas overexpression CD36 stimulated insulin-mediated DNL and lipid droplet formation in vitro. Mechanistically, CD36 was activated by insulin and formed a complex with insulin induced gene-2 (INSIG2), that disrupts the interaction between SREBP cleavage-activating protein (SCAP) and INSIG2, thereby leading to the translocation of SREBP1 from ER to Golgi for processing. Furthermore, treatment with 25-hydroxycholesterol or betulin, molecules shown to enhance SCAP/INSIG interaction, reversed the effects of CD36 on SREBP1 cleavage.

2022-01-03 | GSE191059 | GEO

ALOX15B controls macrophage cholesterol homeostasis via lipid peroxidation, ERK1/2 and SREBP2

Project description:Macrophage cholesterol homeostasis is crucial for health and disease and has been linked to the lipid-peroxidizing enzyme arachidonate 15-lipoxygenase type B (ALOX15B), albeit molecular mechanisms remain obscure. We performed global transcriptome and immunofluorescence analysis in ALOX15B-silenced primary human macrophages and observed a reduction of nuclear sterol regulatory element-binding protein (SREBP) 2, the master transcription factor of cellular cholesterol biosynthesis. Consequently, SREBP2-target gene expression was reduced as were the sterol biosynthetic intermediates desmosterol and lathosterol as well as 25- and 27-hydroxycholesterol. Mechanistically, suppression of ALOX15B reduced lipid peroxidation in primary human macrophages and thereby attenuated activation of mitogen-activated protein kinase ERK1/2, which lowered SREBP2 abundance and activity. Low nuclear SREBP2 rendered both, ALOX15B-silenced and ERK1/2-inhibited macrophages refractory to SREBP2 activation upon blocking the NPC intracellular cholesterol transporter 1. These studies suggest a regulatory mechanism controlling macrophage cholesterol homeostasis based on ALOX15B-mediated lipid peroxidation and concomitant ERK1/2 activation.

2024-04-07 | GSE208160 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data