Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

47 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide expression profiling in bone marrow-derived macrophage (BMM) cells upon RANKL treatment

ABSTRACT: To screen for altered gene expression during osteoclastogenesis, RANKL-treated BMM cells were subjected to gene expression profiling. BMM cells were treated with M-CSF and RANKL for 0, 1, 2 and 3 days. Total RNA was isolated and analyzed by gene expression microarray using the MouseRef-8 v2.0 Expression BeadChip.

ORGANISM(S): Mus musculus

SUBMITTER: Kyunghwan Kim

PROVIDER: E-GEOD-57468 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNA-Seq of osteoclasts derived from female Phlpp1 cKO or control littermates

Project description:Osteoclast progenitors were collected from female Phlpp1 cKO mice or their control littermates and treated with RANKL and M-CSF. On day 4 of cultures when multinucleated cells were present, RNA was collected and RNA-Seq was performed.

2021-05-26 | E-MTAB-10487 | biostudies-arrayexpress

Heme regulates the development of iron-recycling macrophages from monocytes (heme-treated BMM)

Project description:Splenic red pulp macrophages (RPM) degrade senescent erythrocytes and recycle heme-associated iron. The transcription factor Spic is selectively expressed by RPM and is required for their development, but the physiologic stimulus inducing Spic is unknown. Here, we report that Spic also regulated the development of F4/80+VCAM+ bone marrow macrophages (BMM) and that Spic expression in BMM and RPM development was induced by heme, a metabolite of erythrocyte degradation. Pathologic hemolysis induced loss of RPM and BMM due to excess heme but induced Spic in monocytes to generate new RPM and BMM. Spic expression in monocytes was constitutively inhibited by the transcriptional repressor Bach1. Heme induced proteasome-dependent BACH1 degradation and rapid Spic derepression. Further, cysteine-proline dipeptide motifs in BACH1 that mediate heme-dependent degradation were necessary for Spic induction by heme. These findings are the first example of metabolite-driven differentiation of a tissue-resident macrophage subset and provide new insight into iron homeostasis. Global gene expression pattern of bone marrow-derived macrophages generated with GM-CSF in vitro and treated with heme were compared to those treated with vehicle at 6 hours, 24 hours, and 72 hours after treatment. GM-CSF cultures of Spic(igfp/igfp) BM cells were treated with heme (80 Âµm) or vehicle after 6 days in culture. Adherent fraction of cells were harvested 6 hours, 24 hours, and 72 hours after treatment and RNA was isolated using an RNeasy mini kit (Qiagen) and submitted for amplification, labeling and hybridization. Expression values were analyzed after RMA quantile normalization using ArrayStar software (DNASTAR).

2014-03-14 | E-GEOD-46983 | biostudies-arrayexpress

RankL induced mice BMM treated with or without dimethyl itaconate for 24h

Project description:RankL induced mice BMM following dimethyl itaconate treatment for 24h

2022-06-30 | GSE206723 | GEO

Global gene expression profiling using total RNA [BMM, MPI and SPG]

Project description:Differentiation of myeloid progenitor cells leads to distinct populations of mononuclear phagocytes.Various macrophages exhibit distinct biological properties. Here wanted to delineate and characterize gene expression patterns in bone marrow derived macrophages Here wanted to delineate and characterize gene expression patterns in two newly established, self-renewing, in vitro grown non-transformed lines (MPI cells) and in the SP37A3 immature myeloid dendritic cell line. We used microarrays to detail the global programme of gene expression in MPI cells and to compare them to other types of mononuclear phagocytes. [BMM] Total cellular RNA from ex vitro differentiated bone marrow derived macrophages was extracted and hybridized to Affymetrix microarrays to carry out cluster analysis and overlap and gene set analysis for enriched pathways. [MPI and SPG] Total cellular RNA from independently established MPI lines and a splenic immature dendritic cell line was extracted and hybridized to Affymetrix microarrays to carry out cluster analysis and overlap and gene set analysis for enriched pathways.

2013-06-08 | E-GEOD-47473 | biostudies-arrayexpress

Genome-wide expression profiling in bone marrow-derived macrophage (BMM) cells upon RANKL treatment

Project description:To screen for altered gene expression during osteoclastogenesis, RANKL-treated BMM cells were subjected to gene expression profiling.

2014-07-30 | GSE57468 | GEO

Microarray studies on genes stimulated by RANKL in bone marrow macrophages in a cyclooxygenase-2-dependent manner

Project description:Overall goal was to look for the differentially expressed genes between receptor activator of nuclear factor kappa-B ligand (RANKL)-stimulated wild type (WT) bone marrow macrophages (BMMs) and the BMMs in which the expression or the enzyme activity of cyclooxygenase-2 (Cox2), the major enzyme for prostaglandin E2 (PGE2) synthesis, is absent. For this purpose, two separate microarrays (experiment 1 and 2) were done. In both the experiments, Serum Amyloid A3 (Saa3) was one of the most highly differentially expressed gene. For experiment 1, BMMs were isolated from the bone marrow of Cox2 knockout (KO) and WT mice. Out of the three sample groups, two were treated with 30 ng/ml each of macrophage-colony stimulating factor (M-CSF) and RANKL, while the third group was treated with M-CSF only, for 1 day. Two of the sample groups had n=3 biological replicates (i.e. samples), while the third one had n=4 biological replicates. The differential gene expression comparisons among the sample groups were done as (A) WT+MCSF+RANKL_d1 versus Cox2KO+MCSF+RANKL_d1 and (B) WT+MCSF+RANKL_d1 versus WT+MCSF_d1. For experiment 2 also, BMMs were obtained from Cox2 KO and WT mice. All the four sample groups were treated with M-CSF and RANKL for 3 days. All the four sample groups had n=4 biological replicates. One of the WT sample group was also treated with an inhibitor of Cox2 activity,NS398 (0.1 Âµm) and one of the KO sample group was also treated with the product of Cox2 enzyme, PGE2 (1 Âµm). The differential gene expression comparisons among the sample groups were done as (A) WT+MCSF+RANKL_d3 versus Cox2KO+MCSF+RANKL_d3; (B) WT+MCSF+RANKL_d3 versus WT+MCSF+RANKL+NS398_d3 and (C) Cox2KO+MCSF+RANKL+PGE2_d3 versus Cox2KO+MCSF+RANKL_d3.

2016-01-07 | E-GEOD-72047 | biostudies-arrayexpress

Interferon gamma down-regulates miR-3473b to promote macrophage activation

Project description:Macrophages are major effector cells and antigen presenting cells of the innate immune system and classical activation of macrophage function requires interferon–γ (IFN-γ) pretreatment (priming) and TLR stimuli, which promotes inflammatory responses though high levels of pro-inflammatory cytokines and lower level of the anti-inflammatory cytokines, resulting in microbicidal and tumoricidal effect. However, the underlying molecular mechanism of IFN-γ priming remains elusive. In this study, we explored the effect of IFN-γ on macrophages at miRNA level and discovered that miR-3473b, which was down-regulated after IFN-γ priming, could attenuate the priming effect of IFN-γ. Molecular study revealed that miR-3473b promoted Akt/GSK3 signaling and IL-10 production through directly targeting PTEN to suppress inflammatory response and tumor-suppressing capability of macrophages. In summary, our data demonstrate that IFN-γ beef up macrophage inflammatory response and tumor suppressing capacity by limiting miR-3473b-mediated PTEN suppression. Our work identified an IFN-γ/miR-3473b/Akt axis in the regulation of macrophage function and activation. the assay was performed with 5 μg total RNA samples from both normal BMM (labeled by Cy3) and BMM primed by IFN-γ (100U/ml) for 4 h(labeled by Cy5), normal BMM serves as control.

2014-10-01 | E-GEOD-50569 | biostudies-arrayexpress

miRNA in mouse macrophages

Project description:By employing miRCURY LNAM-bM-^DM-" microRNA Array, we have identified a subset of 21 top miRNAs that are differentially expressed between GM-BMM and M-BMM cells To know the differential expression of miRNA in mouse GM-CSF-induced bone marrow-derived macrophages (GM-BMM) vs. M-CSF-induced BMM (M-BMM)

2013-04-17 | E-GEOD-46085 | biostudies-arrayexpress

Transcription profiling of bone marrow derived cells from mice stimulated with RANKL to generate osteoclasts in a time series

Project description:Bone marrow derived cells stimulated with RANKL (receptor activator of nuclear factor kappa B ligand, also known as Tumor necrosis factor ligand superfamily member 11) to generate osteoclasts.

2007-06-06 | E-TABM-212 | biostudies-arrayexpress

Transcriptional responses of mouse bone marrow-derived macrophages (BMM) to lipopolysaccharide (LPS) - Illumina arrays

Project description:These microarrays were performed for use in a genome-wide scan for LPS-regulated genes in mouse macrophages, in order to construct a list of LPS-regulated genes for detailed interrogation on custom microarrays (see GSE19490 for custom array analysis). Mouse macrophages (bone marrow-derived macrophages, BMM) were stimulated with the TLR4 agonist, lipopolysaccharide, over a time course (0, 0.5, 2, 6, 24h) and analysed in biological duplicate by commercial Illumina microarray.

2012-03-28 | E-GEOD-19766 | biostudies-arrayexpress

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