Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NOTCH2 Promotes Osteoclast Maturation and Metabolism and Modulates the Transcriptome Profile During Osteoclastogenesis

ABSTRACT: Bone marrow derived macrophages (BMM) from Notch2tm1.1Ecan, harboring a NOTCH2 gain-of-function mutation, and control mice were cultured with macrophage colony stimulating factor (M-CSF) and receptor activator of NF-kB ligand (RANKL). Bulk RNA-Seq revealed enhanced cell metabolism, aerobic respiration, and mitochondrial function, all associated with osteoclastogenesis, in Notch2tm1.1Ecan cells. Single cell RNA-Seq data of BMMs treated with M-CSF or M-CSF and RANKL for 3 days identified 11 well-defined cellular clusters. There was an increased number of cells expressing gene markers associated with the osteoclast and with related clusters in Notch2tm1.1Ecan than in control BMMs.

ORGANISM(S): Mus musculus

PROVIDER: GSE248138 | GEO | 2024/01/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

NOTCH2 Promotes Osteoclast Maturation and Metabolism and Modulates the Transcriptome Profile During Osteoclastogenesis

Project description:Bone marrow derived macrophages (BMM) from Notch2tm1.1Ecan, harboring a NOTCH2 gain-of-function mutation, and control mice were cultured with macrophage colony stimulating factor (M-CSF) and receptor activator of NF-kB ligand (RANKL). Bulk RNA-Seq revealed enhanced cell metabolism, aerobic respiration, and mitochondrial function, all associated with osteoclastogenesis, in Notch2tm1.1Ecan cells. Single cell RNA-Seq data of BMMs treated with M-CSF or M-CSF and RANKL for 3 days identified 11 well-defined cellular clusters. There was an increased number of cells expressing gene markers associated with the osteoclast and with related clusters in Notch2tm1.1Ecan than in control BMMs.

2024-01-03 | GSE248137 | GEO

Profiling of DNA Methylation during RANKL Induced Osteoclastogenesis using Whole-Genome Bisulfite Sequencing

Project description:Purpose: The goals of this study are to describe the DNA methylation profile during RANKL induced osteoclastogenesis. Methods: Primary bone marrow cells were isolated and treated with M-CSF (30ng/mL) to generate bone marrow macrophages (BMMs). BMMs were then used to generate preosteoclast (pOC) stimulated by M-CSF (30ng/mL) together with RANKL (100ng/mL) for 24 h and mature osteoclast (mOC) stimulated by M-CSF (30ng/mL) together with RANKL (100ng/mL) for 72 h or more. DNA methylation profiles of BMM, pOC and mOC were generated by deep sequencing, using Illumina NovaSeq 6000. Results: After acquiring of clean reads, we used Hisat2 for spliced mapping. We mapped about 40 million sequence reads per sample of the WGBS results. Saturation rate analysis was then performed evaluating the gene coverage rate along with read depth increase. The transcripts mapping to difference functional region of the genome was then analyzed. Circos software was used to map the consistency of samples with mouse genome on a chromosomal level. The quantification of transcript intensity was analyzed using RPKM (Reads Per Kb per Million reads). Conclusions: Our study represents the first high-throughput WGBS sequencing data of DNA methylation during osteoclastogenesis.

2020-06-04 | GSE133515 | GEO

Effect of GDF11 on RANKL-induced osteoclastogenesis

Project description:GDF11 treatment leads to bone loss in mice and strongly stimulates RANKL-induced osteoclastogenesis of bone marrow-derived macrophages (BMMs) in vitro. We used microarrays to identified distinct classes of up-regulated genes in BMMs after GDF11 treatment. Mouse BMMs were treated with or without GDF11 for RNA extraction and and hybridization on Affymetrix microarrays

2016-07-21 | E-GEOD-84609 | biostudies-arrayexpress

Abeliophyllum distichum Nakai Extract exerts anti-osteoporotic effects by suppressing RANKL-induced osteoclastogenesis

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

2020-09-23 | GSE152479 | GEO

Ethyl acetate fraction of Lentinula edodes (LEA) inhibits osteoclastogenesis by suppressing NFATc1 expression

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

2020-02-24 | GSE142866 | GEO

Effect of GDF11 on RANKL-induced osteoclastogenesis

Project description:GDF11 treatment leads to bone loss in mice and strongly stimulates RANKL-induced osteoclastogenesis of bone marrow–derived macrophages (BMMs) in vitro. We used microarrays to identified distinct classes of up-regulated genes in BMMs after GDF11 treatment.

2016-07-21 | GSE84609 | GEO

Murine Bone Marrow Macrophages: Control vs. RANKL Stimulated

Project description:To identify the microRNAs that are involved in osteoclastogenesis, microRNA expression profiles in mouse bone marrow macrophages (BMMs) stimulated with RANKL (BMOc) were compared with that of control untreated BMMs. These results provide insights into the mechanisms to regulate osteoclastogenesis and bone resorption activities in osteoclasts by microRNA. BMMs were cultured with 20 ng/ml M-CSF in the presence or absence of 50 ng/ml RANKL for 24 hours. Cells were collected for total RNA isolation, and were subjected to microRNA array analysis.

2013-07-10 | E-GEOD-48629 | biostudies-arrayexpress

TMBIM6 deficiency leads to bone loss by accelerating osteoclastogenesis

Project description:To screen for altered gene expression during osteoclastogenesis, BMM cells depleted of TMBIM6 with or without RANKL were subjected to gene expression profiling.

2023-07-10 | GSE231889 | GEO

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. 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.

2014-07-30 | E-GEOD-57468 | biostudies-arrayexpress

M-CSF priming of osteoclast precursors can cause osteoclastogenesis-insensitivity, which can be prevented and overcome on bone

Project description:Comparison of gene expression of the osteoclast precursor myeloid blast seeded on plastic and on bone, primed with M-CSF for 4 days and culture with M-CSF and RANKL for 1 day. Osteoclasts and macrophages share progenitors that must receive decisive lineage signals driving them into their respective differentiation routes. Macrophage colony stimulation factor M-CSF is a common factor; bone is likely the stimulus for osteoclast differentiation. To elucidate the effect of both, shared mouse bone marrow precursor myeloid blast was pre-cultured with M-CSF on plastic and on bone. M-CSF priming prior to stimulation with M-CSF and osteoclast differentiation factor RANKL resulted in a complete loss of osteoclastogenic potential without bone. This coincided with a steeply decreased expression of osteoclast genes TRACP and DC-STAMP, but an increased expression of the macrophage markers F4/80 and CD11b. Compellingly, M-CSF priming on bone accelerated the osteoclastogenic potential: M-CSF primed cells that had received only one day M-CSF and RANKL and were grown on bone already expressed an array of genes that are associated with osteoclast differentiation and these cells differentiated into osteoclasts within 2 days. This implies that adhesion to bone dictates the fate of osteoclast precursors. Common macrophage-osteoclast precursors may become insensitive to differentiate into osteoclasts and regain osteoclastogenesis when bound to bone or when in the vicinity of bone. Two conditions: Osteoclast precursors on plastic and on bone, n=4, dye swap

2014-06-02 | E-GEOD-58146 | 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