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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE72047 | GEO | 2016/01/07

SECONDARY ACCESSION(S): PRJNA292819

REPOSITORIES: GEO

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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

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

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

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

2013-07-10 | GSE48629 | GEO

Gene Expression Profile identify a role for cyclooxygenase 2-depedent prostinoid generation in BMP6-induced

Project description:The bone morphogenetic protein (BMP) family of proteins participates in an underappreciated signaling pathway involved in regulating angiogensis in physiological and pathological conditions. Microarray profiles of BMP-responsive genes in the endothelium performed by our lab suggest important roles for cyclooxygenase-2 (Cox2) as a potential downstream regulator of BMP-induced angiogenesis. Cox2 is upregulated by BMP6 at both mRNA and protein levels. Inhibition of Cox2 blocks BMP6 induced endothelial cell proliferation, migration and tube formation activity. Microvessel outgrowth stimulated by BMP6 also required Cox2 activity. These results strongly support that Cox2 is an important downstream target for BMP6, and that prostaniod synthesis is essential for BMP6 induced endothelial cell activation. This further suggests that our microarray data is a reliable tool to identify unkown BMP6 targets in angiogenesis. Keywords: BMP, angiogenesis, Cox2, MEC

2006-12-31 | GSE4909 | GEO

The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury byparacrine signaling

Project description:Paracrine signals play pivotal roles in organ homeostasis. Mesenchymal stromal cells (MSCs) play a key role in regulating epithelium homeostasis in the intestine while their paracrine effects are poorly characterized. Here, we identified prostaglandin E2 (PGE2) secreted by cyclooxygenase (COX)-expressing MSCs as a vital factor to maintain the intestinal mucosal barrier. We found that MSCs-induced organoid swelling through paracrine effect in vitro, a process due to enhanced water adsorption and is mediated by the COX-PGE2-EP4 axis. To further explore the regulatory effect of this axis on the intestinal epithelial barrier in vivo, we established the conditional knockout mouse model to specifically delete COX in MSCs and found that PGE2 reduction downregulated the gene Muc2 and induced a gastric metaplasia-like phenotype. Moreover, PGE2 defects increased the susceptibility of intestinal epithelium to colitis. Our study uncovers the paracrine signaling of COX-expressing MSCs in intestinal mucosal barrier maintenance, providing a basis for understanding the role of mesenchymal cells in the psychophysiology function of the intestine.

2023-09-26 | GSE243704 | 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

Differential gene expression analysis of PTGS2-inducing and PTGS2-non-inducing oropharyngeal carcinoma cell lines.

Project description:Prostaglandin E2 (PGE2) is a powerful immunomodulator synthesized by the COX2 enzyme, coded by human gene PTGS2. PGE2 is known to possess angiogenic, protumor and immunosuppressive functionality in the microenviornment of oropharyngeal carcinomas (OPC). Differential induction of PTGS2 in infiltrating myeloid-derived immunocytes has been observed with media conditioned by cultured OPC biopsies and OPC-derived cell lines alike. To identify PTGS2-inducing, OPC-derived gene products, we utilized bluk RNA sequencing on 4 OPC-derived cell lines to compare expression profiles of PTGS2-inducing (SCC154, SCC25) with that of PTGS2-non-inducing (2A3, SCC152) cell lines. Interleukin-1α (IL-1α) was among the differentially expressed candidates between cell lines.

2022-10-21 | GSE215973 | GEO

Comparative characterization of osteoclasts derived from murine bone marrow macrophages and RAW 264.7 cells using quantitative proteomics

Project description:Osteoclasts (OCs) are bone-resorbing cells differentiated from macrophage/monocyte precursors in response to M-CSF and RANKL. In vitro models are principally based on primary bone marrow macrophages, but RAW 264.7 cells are frequently used because they are widely available, easy to culture, and more amenable to genetic manipulation than primary cells. Increasing evidence, however, has shown that the vastly different origins of these two cell types may have important effects on cell behavior. In particular, M-CSF is prerequisite for the differentiation of BMMs, by promoting survival and proliferation and priming the cells for RANKL induction. RAW 264.7 cells readily form OCs in the presence of RANKL, but M-CSF is not required. Based on these key differences, we sought to understand their functional implications and how it might affect osteoclast differentiation and related signaling pathways. Using a robust and high-throughput proteomics strategy, we quantified the global protein changes in OCs derived from bone marrow macrophages and RAW 264.7 cells at 1, 3, and 5 days of differentiation. Correlation analysis of the proteomes demonstrated low concordance between the two cell types (R2 ≈ 0.13). Bioinformatics analysis indicate that RANKL-dependent signaling was intact in RAW 264.7 cells, but biological processes known to be dependent on M-CSF were significantly different; including cell cycle control, cytoskeletal organization, and apoptosis. RAW 264.7 cells exhibited constitutive activation of Erk and Akt that was dependent on the activity of Abelson tyrosine kinase, and the timing of Erk and Akt activation was significantly different between BMMs and RAW 264.7 cells. Our findings provide the first evidence for major differences between BMMs and RAW 264.7 cells, indicating that careful consideration is needed when using the RAW 264.7 cell line when studying M-CSF-dependent signaling and functions.

2018-11-27 | PXD009610 | Pride

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