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Expression data from polarized macrophages: effect of p53

ABSTRACT: p53 is critically important in preventing oncogenesis but its role in non-cancer biology remains unclear. Macrophages exist as two subtypes (M1 and M2). Nutlin-3a (p53 activator) inhibits M2 gene expression and phenotype. p53 acts by suppressing transcription of c-Myc and thence regulates expression of a subset of M2 markers. This work has implications for our understanding of the mechanisms that regulate plasticity of macrophages in health and disease. We used microarrays to study the global programme of gene expression in nutlin-3a and 10058F4 (C-myc inhibitor) treated polarised mouse macrophages 5 groups of cultured mouse macrophages: (i) M0 (untreated), (ii) M1, (iii) M2, (iv) M2+nutlin-3a, (v) M2+MYC inhibitor (10058F4). 3 biological replicates per treatment group.

ORGANISM(S): Mus musculus

SUBMITTER: Ling Li

PROVIDER: E-GEOD-53321 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A unique role for p53 in the regulation of M2 macrophage polarization.

Li L L Ng D S W DS Mah W-C WC Almeida F F FF Rahmat S A SA Rao V K VK Leow S C SC Laudisi F F Peh M T MT Goh A M AM Lim J S Y JS Wright G D GD Mortellaro A A Taneja R R Ginhoux F F Lee C G CG Moore P K PK Lane D P DP

Cell death and differentiation 20141219 7

P53 is critically important in preventing oncogenesis but its role in inflammation in general and in the function of inflammatory macrophages in particular is not clear. Here, we show that bone marrow-derived macrophages exhibit endogenous p53 activity, which is increased when macrophages are polarized to the M2 (alternatively activated macrophage) subtype. This leads to reduced expression of M2 genes. Nutlin-3a, which destabilizes the p53/MDM2 (mouse double minute 2 homolog) complex, promotes p ...[more]

PMID: 25526089

Similar Datasets

Expression data from polarized macrophages: effect of p53

Project description:p53 is critically important in preventing oncogenesis but its role in non-cancer biology remains unclear. Macrophages exist as two subtypes (M1 and M2). Nutlin-3a (p53 activator) inhibits M2 gene expression and phenotype. p53 acts by suppressing transcription of c-Myc and thence regulates expression of a subset of M2 markers. This work has implications for our understanding of the mechanisms that regulate plasticity of macrophages in health and disease. We used microarrays to study the global programme of gene expression in nutlin-3a and 10058F4 (C-myc inhibitor) treated polarised mouse macrophages

2015-01-01 | GSE53321 | GEO

Quantitative proteomic analysis of four subtypes of M2 macrophages

Project description:In this study, we used mass spectrometry and label-free quantification (LFQ) to characterize the global proteomics of polarized (M1, M2a, M2b, M2c, and M2d) and unpolarized (M0) phenotypes of macrophages from human THP-1 monocytes. The results described the biological functions of the four M2 macrophages subtypes and provided available references for identifying M2 macrophages or subtypes of M2 macrophages.

2022-08-12 | PXD022320 | Pride

Genome-wide analysis of M1 and M2 polarized macrophages with CNI-1493 treatment

Project description:Analysis of the effects of CNI-1493 treatment on M1 and M2 polarized macrophages. The purpose of this microarray is to identify genes that may be differentially expressed in M1 or M2 macrophages after treatment with CNI-1493. CNI-1493 is a known inhibitor of M1 macrophages but details of its molecular mechanism are unknown. The effect of CNI-1493 on M2 macrophages has yet to be explored, but we hypothesize that CNI-1493 treatment will attenuate pro-tumor properties of M2 macrophages. We demonstrate with this array that known macrophage markers are unchanged after treatment with CNI-1493, indicating that CNI-1493 does not change the macrophage phenotype on a transcriptional level. Additionally, no candidate genes to suggest how CNI-1493 may attenuate the pro-tumor effects of M2 macrophages are readily identifiable. Total RNA extracted from M1 or M2 macrophages after polarization with GM-CSF (25ng/ml) or M-CSF (25ng/ml) for 7 days, followed by addition of IFN-γ (20ng/ml) and LPS (100ng/ml) or IL-4 (40ng/ml) for 18 hours, respectively, from CD14+ human PBMCs, and treated with CNI-1493 (200nM)

2015-03-12 | E-GEOD-66805 | biostudies-arrayexpress

MSModDetector: A Tool for Detecting Mass Shifts and Post-Translational Modifications in Individual Ion Mass Spectrometry Data

Project description:Intact mass spectrometry analysis of endogenous p53 immunoprecipitated from MCF7 cells responding to nutlin-3a or ultraviolet irradiation.

2023-03-13 | MSV000091481 | MassIVE

Discovery of the p53 targetome in MCF7 cells from ChIP-Seq data

Project description:RNA-seq and ChIP-seq on MCF-7 breast cancer cell line upon activation of p53 by the non-genotoxic small molecule Nutlin-3a ChIP-seq on p53 in MCF7 with Nutlin-3a stimulation (S) in triplicate, and the control (input), in stimulated and non stimulated, using illumina HiSeq 2000

2014-05-27 | E-GEOD-47041 | biostudies-arrayexpress

Expression data from human sarcoma patient samples treated with either vehicle control or Nutlin-3a

Project description:This study has examined the molecular mechanisms underlying sensitivity of sarcomas to Nutlin-3a, a non-genotoxic activator of the p53 pathway. Human patient material was collected immediately following surgical resection, dissected into small pieces and ex planted onto gelatin sponges immersed in media containing either vehicle control or Nutlin-3a (10uM and/or 50uM) for 48 hours. Nutlin-3a represents a novel targeted therapy for the treatment of sarcomas. We have examined expression profiles of genes upregulated in sarcoma patient derived tissues following nutlin-3a treatment ex vivo 16 samples ((Vehicle control and Nutlin-3a (10uM and 50uM) treated samples)) from 6 sarcoma patients

2014-03-10 | E-GEOD-48296 | biostudies-arrayexpress

Interruption of p53-MDM2 Interaction by Nutlin-3a in Human Lymphoma Cell Models Initiates a Cell-Dependent Global Effect on Transcriptome and Proteome Level

Project description:In most lymphomas, p53 signaling pathway is inactivated by various mechanisms independent to p53 gene mutations or deletions. In many cases, p53 function is largely regulated by alterations in the protein abundance levels by the action of E3 ubiquitin-protein ligase MDM2, targeting p53 to proteasome-mediated degradation. In the present study, an integrating transcriptomics and pro-teomics analysis was employed to investigate the effect of p53 activation by a small-molecule MDM2-antagonist, nutlin 3a, on three lymphoma cell models following p53 activation. Our analy-sis revealed a system-wide nutlin 3a-associated effect in all examined lymphoma types, identifying in total of 4037 differentially affected proteins involved in a plethora of pathways, with significant heterogeneity among lymphomas. Our findings include known p53-targets and novel p53 activa-tion effects, involving transcription, translation, or degradation of protein components of path-ways, such as a decrease in key members of PI3K/mTOR pathway, heat-shock response, and gly-colysis, and an increase in key members of oxidative phoshosphorylation, autophagy and mito-chondrial translation. Combined inhibition of HSP90 or PI3K/mTOR pathway with nutlin 3a-mediated p53-activation enhanced the apoptotic effects suggesting a promising strategy against human lymphomas. Integrated omic profiling after p53 activation offered novel insights on the regulatory role specific proteins and pathways may have in lymphomagenesis.

2023-07-30 | PXD009290 | Pride

Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) of BJ cells treated with Nutlin-3a, an MDM2 inhibitor, which induces p53.

Project description:We applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells in which p53 was induced by Nutlin-3a RNA-seq, using Illumina HiSeq 2000, was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs Ribosome profiling was applied to BJ cells treated with Nutlin-3a, at 5 timepoints: 0, 2, 4, 6, 19 hrs

2013-06-01 | E-GEOD-45785 | biostudies-arrayexpress

Discovery of the p53 targetome in MCF7 cells from RNA-seq data

Project description:RNA-seq and ChIP-seq on MCF-7 breast cancer cell line upon activation of p53 by the non-genotoxic small molecule Nutlin-3a RNA-seq on MCF7 without (NS) or with Nutlin-3a stimulation (S), in duplicate, using illumina HiSeq 2000

2014-05-27 | E-GEOD-47042 | biostudies-arrayexpress

RNA-seq analysis identifies regulators of macrophage reprogramming from M2 to M1-like phenotype

Project description:We analyzed expression profiles of thioglyolate elicted peritoneal exudate cells (peritoneal macrophages). Peritoneal macrophages were polarized into M1 and M2 macrophages by activation with IFNgamma+ LPS and Il4, respectively. We predicted a gene-regulatory network, which consists of four transcription factors (E2f1,Myc, Stat6, Pparg) regulating metabolic genes, M1 and M2-associated genes. The predicted regulators were all active in M2 macrophages. We hypothesized that these transcription factors are essential regulators to maintain M2 phenotype. To further validate our findings, we treated M2-polarized macrophages with siRNA-pools targeting E2f1, Myc, Stat6 and Pparg. In this study, we observed a switch towards an M1-like phenotype after transfection of siRNA-pools. In addition, Inflammatory pathways were upreguated while fatty acid metabolism was down regulated.

2020-01-27 | GSE129253 | GEO

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