Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles of GPR15 knock out macrophages

ABSTRACT: To confirm the changed gene expression profiles in GPR15 knock out (KO) macrophages, we applied a SurePrint G3 Mouse Gene Expression service from Takara Bio Inc (Kusatsu, Shiga, Japan) to analyze gene expression profiles in lipopolysaccharide (LPS)-stimulated GPR15KO macrophages, comparing with wild type (WT) macrophages. Most significantly up-regulated genes in GPR15KO macropahges included Il6, Il17a, Il23, Tnfsf8, Il1b, Ifna2 and Ccnd2. On the contrary, several inflammation-related genes, including Ccl17, Itgax, Nrp1 and Rasgrf2, were down-regulated in WT macrophages, compared to GPR15 KO macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE86020 | GEO | 2016/08/25

SECONDARY ACCESSION(S): PRJNA339993

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiles of GPR15 knock out macrophages

Project description:To confirm the changed gene expression profiles in GPR15 knock out (KO) macrophages, we applied a SurePrint G3 Mouse Gene Expression service from Takara Bio Inc (Kusatsu, Shiga, Japan) to analyze gene expression profiles in lipopolysaccharide (LPS)-stimulated GPR15KO macrophages, comparing with wild type (WT) macrophages. Most significantly up-regulated genes in GPR15KO macropahges included Il6, Il17a, Il23, Tnfsf8, Il1b, Ifna2 and Ccnd2. On the contrary, several inflammation-related genes, including Ccl17, Itgax, Nrp1 and Rasgrf2, were down-regulated in WT macrophages, compared to GPR15 KO macrophages. Abdominal macrophages from WT and GPR15 KO mice were stimulated with PBS or LPS (100 ng/ml) for 4 hrs. Total RNA were extracted using a TRIzol-chloroform based method.

2016-08-25 | E-GEOD-86020 | biostudies-arrayexpress

GPR15+ vs GPR15- tumor-associated Tregs

Project description:GPR15+ vs GPR15- tumor-associated Tregs were sorted from colorectal cancer mice (Foxp3-RFP x GPR15-GFP)

2021-03-12 | GSE168744 | GEO

Expression data from GPR15+CD4+ and GPR15-CD4+ T cells in LILP

Project description:GPR15 is an orphan G-protein coupled receptor and its expression is abundant among T cells in the large intestine lamina propria. We used microarrays to examine charateristics of GPR15- vs GPR15+ CD4+ T cells in LILP and identified distinct classes of up-regulated genes in GPR15+ CD4+ T cells. We have generated GFP knock-in mice in GPR15 locus and used GFP as a maker for GPR15 expression. In heterozygous mice, GPR15+CD4+ T cells and GPR15-CD4-T cells were sorted and RNA was prepared from them.

2013-05-09 | E-GEOD-45773 | biostudies-arrayexpress

Expression data from GPR15+CD4+ and GPR15-CD4+ T cells in LILP

2013-05-09 | GSE45773 | GEO

GPR15+ vs GPR15- tumor-associated Tregs

Project description:GPR15+ vs GPR15- tumor-associated Tregs

| PRJNA713801 | ENA

Specific induction of GPR15 expression in heterogeneous blood lymphocytes by smoking

Project description:Although a mucosal and cutaneous chemokine ligand for G protein –linked receptor GPR15 was recently identified, the physiological role of GPR15 remains yet elusive. In blood, in has been shown that smoking is, to date, the only specific condition leading to an increase in GPR15+ T cells. We therefore used transcriptome sequencing to describe GPR15-expressing blood T cells in more detail.

2019-01-04 | GSE114837 | GEO

Ahr-Foxp3-RORγt Axis Controls Gut Homing of CD4+ T Cells by Regulating GPR15

Project description:The orphan chemoattractant receptor GPR15 is important for homing T lymphocytes to the large intestine, thereby maintaining intestinal immune homeostasis. However, the molecular mechanisms underlying the regulation of GPR15 expression remain elusive. Here we show a central role of the aryl hydrocarbon receptor (Ahr) in promoting GPR15 expression both in mice and human, thus gut homing of T lymphocytes. Mechanistically, Ahr directly binds to open chromatin regions of the Gpr15 locus to enhance its expression. Ahr transcriptional activity in directing GPR15 expression was modulated by two transcription factors, Foxp3 and RORγt, both of which are expressed preferentially by gut Tregs in vivo. Specifically, Foxp3 interacted with Ahr and enhanced Ahr DNA binding at the Gpr15 locus, thereby promoting GPR15 expression. In contrast, RORγt plays an inhibitory role at least in part by competing with Ahr binding to the Gpr15 locus. Our findings thus demonstrate a key role for Ahr in regulating Treg intestinal homing under the steady state and during inflammation, and the importance of Ahr-RORγt-Foxp3 axis in regulating gut homing receptor GPR15 expression by lymphocytes.

2020-07-29 | GSE137171 | GEO

GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome

Project description:Viral myocarditis is characterised by infiltration of mononuclear cells essential for virus elimination. GPR15 has been identified as a homing receptor for regulatory T cells in inflammatory intestine diseases, but its role in inflammatory heart diseases is still elusive. Therefore, we investigated the role of GPR15 during coxsackievirus B3‑induced myocarditis utilizing GPR15‑deficient mice as well as using in vitro experiments. Here we show that GPR15 deficiency had no effect on susceptibility to virus infection, but virus elimination was scant leading to adverse cardiac remodelling and impaired cardiac function. Delayed recruitment of regulatory T cells was accompanied by prolonged persistence of cytotoxic T cells as well as regulatory T cells in GPR15-deficient mice. Further, RNA sequencing revealed prolonged inflammatory response and altered chemotaxis in GPR15-deficient mice. In line, we identified GPR15 and its ligand GPR15L as an important chemokine receptor-ligand pair for the recruitment of regulatory and cytotoxic T cells. In summary, the insufficient virus elimination might be caused by a delayed recruitment of T cells as well as delayed interferon-γ expression, resulting in a prolonged inflammatory response and an adverse outcome in GPR15-deficient mice.

2023-11-24 | GSE248521 | GEO

Smoking induced expression of the GPR15 gene indicates its potential role in chronic inflammatory pathologies

Project description:The aim of present study was to study the changes in peripheral blood gene expression profile induced by smoking. RNA was extracted from the PBMCs of 48 persons with detailed smoking history (24 were non-smokers, 16 were current smokers and 8 were ex-smokers). Gene expression profile was evaluated with the RNA sequencing and results were analyzed separately in males (24) and females (24). In male smokers, 13 genes were statistically significantly (FDR < 0.1) differentially expressed. In female smoker, 5 genes were differentially expressed with the FDR<0.1. Most of the differentially expressed genes were different between male and female smokers. However, GPR15, expression was changed in male and female smokers compared to non-smokers. Further analysis on the methylation of the genes GPR15 identified significant hypomethylation in smokers compared to non-smokers. GPR15 is the chemo-attractant receptor that regulates T-cell migration and immunity. Up-regulation of GPR15 could explain to some extend the health hazards of smoking for chronic inflammatory diseases

2018-04-30 | GSE68549 | GEO

Gene expression data from WT and SREBP-1a deficient macrophages

Project description:Gene expression from bone-marrow drived macrophages of WT and SREBP-1a deficient mice RNAs were collected 6 different macropahges and pooled RNA for microarray

2011-03-22 | E-GEOD-28037 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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