Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

54 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of LPS-stimulated macrophages in wild-type and LysM-Cre+;Akirin2fl/fl mice

ABSTRACT: Akirin2 is an evolutionally conserved nuclear protein involved in the regulation of a set of inflammatory gene expression in various cell types. We used microarrays to examine the effect of Akirin2 deficiency in LPS-inducible gene expression in macrophages Peritoneal macrophages from wild-type and LysM-Cre+;Akirin2fl/fl mice were stimulated with LPS for 0, 2 and 4 hours, followed by RNA extraction and microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Osamu Takeuchi

PROVIDER: E-GEOD-59319 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of mouse LPS-stimulated macrophages from wild-type and Zc3h12a-/- knockouts

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, induces the expression of various genes including proinflammatory cytokines, and the expression is modified by the presence of Zc3h12a. We used microarrays to examine influence of Zc3h12a deficiency in LPS-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type and Zc3h12a-/- mice were stimulated with LPS for 0, 1, 2 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2009-03-01 | E-GEOD-14891 | biostudies-arrayexpress

Transcription profiling of mouse LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- animals

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, activates intracellular signaling via adaptors, MyD88 and TRIF, leading to the expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of MyD88 or TRIF deficiency in LPS-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2009-03-01 | E-GEOD-14890 | biostudies-arrayexpress

Transcription profiling by array of LysMCre/Cre and KLF2?/? (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with lipopolysaccharide (LPS) for 6 hours

Project description:Gene expression profile of LysMCre/Cre and KLF2?/? primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2?/? primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation. We injected 3 pairs of LysMCre/Cre (n=3) and KLF2?/? (n=3) mice with 2 ml of thioglycolate broth intraperitoneally. After 72 hours of thioglycolate injection, total cell suspension from peritoneal cavity were collected. These cells were seeded on 100mm tissue culture plates. Cells were allowed to attach for 4 hours and unattached cells were removed by washing with cell culture medium. These cells were placed in humidified incubator for additional 24 hours before LPS treatment. LPS was diluted to final concentration of 100ng/ml in culture medium and this medium was placed on peritoneal macrophages derived from LysM Cre/Cre and KLF2?/? mice for 6hours. Cells were lysed and total RNA was isolated and subjected to hybridization on Affymetrix microarrays.

2012-04-15 | E-GEOD-26727 | biostudies-arrayexpress

Expression data of LPS-stimulated macrophages in wild-type and LysM-Cre+;Akirin2fl/fl mice

Project description:Akirin2 is an evolutionally conserved nuclear protein involved in the regulation of a set of inflammatory gene expression in various cell types. We used microarrays to examine the effect of Akirin2 deficiency in LPS-inducible gene expression in macrophages

2014-07-11 | GSE59319 | GEO

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

Tissue-specific differences in PPARγ control of macrophage function.

Project description:PPARγ is known for its anti-inflammatory actions in macrophages. However, which macrophage populations express PPARγ in vivo and how it regulates tissue homeostasis in the steady state and during inflammation is not completely understood. We show that lung and spleen macrophages constitutively expressed PPARγ, while other macrophage populations did not. Recruitment of monocytes to sites of inflammation was associated with induction of PPARγ as they differentiated to macrophages. Its absence in these macrophages led to failed resolution of inflammation, characterized by persistent, low-level recruitment of leukocytes. Conversely, PPARγ agonists supported an earlier cessation in leukocyte recruitment during resolution of acute inflammation and likewise suppressed monocyte recruitment to chronically inflamed atherosclerotic vessels. In the steady state, PPARγ deficiency in macrophages had no obvious impact in the spleen but profoundly altered cellular lipid homeostasis in lung macrophages. Reminiscent of pulmonary alveolar proteinosis, LysM-Cre x PPARγflox/flox mice displayed mild leukocytic inflammation in the steady-state lung and succumbed faster to mortality upon infection with S. pneumoniae. Surprisingly, this mortality was not due to overly exuberant inflammation, but instead to impaired bacterial clearance. Thus, in addition to its anti-inflammatory role in promoting resolution of inflammation, PPARγ sustains functionality in lung macrophages and thereby has a pivotal role in supporting pulmonary host defense. The two major subsets of monocytes (Ly-6C+ and Ly-6Clo) from 12-week old C57Bl/6 mice were sorted and the RNA extracted and hybridized to Affymetrix GeneChip® 430 2.0 arrays. We pooled leukocytes from 5 mice for each sort and sorted 3 to 4 separate times for 3 to 4 biological replicates.

2012-10-03 | E-GEOD-32034 | biostudies-arrayexpress

Expression data from LysMCre/Cre and KLF2∆/∆ (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with LPS for 6hours

Project description:Gene expression profile of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation.

2012-04-16 | GSE26727 | GEO

RNA-seq analysis of Mettl3fl/fl and LysM-cre, Mettl3fl/fl BMDMs (bone-marrow-derived macrophages) Transcriptomes

Project description:To comprehensively learn about the mechanisms of METTL3-mediated pro-tumoral functions, we performed RNA-sequencing to identify differentially expressed genes in bone-marrow-derived macrophages (BMDMs) in Mettl3fl/fl (WT) and LysM-cre, Mettl3fl/fl (KO) mice after co-cultured with MC38 cell line.

2022-01-01 | GSE182865 | GEO

Transcription profiling of mouse MALP-2-stimulated macrophages FROM wild-TYPE, IRAK-2-/- AND IRAK-1-/IRAK-2-/- animals

Project description:IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of IRAK-2 or IRAK-1/IRAK-2 deficiency in MALP-2-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, IRAK-2-/- and IRAK-1/IRAK-2 mice were stimulated with MALP-2 for 0, 2, 4, and 8 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2008-04-05 | E-GEOD-10765 | biostudies-arrayexpress

RNA-seq analysis of Mettl3fl/fl and LysM-cre, Mettl3fl/fl MDSC Transcriptomes

Project description:To comprehensively learn about the mechanisms of METTL3-mediated pro-tumoral functions, we performed RNA-sequencing to identify differentially expressed genes in isolated MDSC in Mettl3fl/fl (WT) and LysM-cre, Mettl3fl/fl (KO) MC38-bearing mice

2022-01-01 | GSE182864 | 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