Similar Datasets
Project description:We reported exosome-guided phenotype switches between M1- and M2-polarized BMDMs. M1- or M2-polarized BMDMs were successfully reprogrammed to M2- or M1-phenotype via the treatment of exosomes obtained from M2- or M1-polarized BMDMs. In this uploaded information, the exosomes from M1- and M2-polarized BMDMs were analyzed by high-throughput sequencing.
2022-03-02 | GSE179172 | GEO
Project description:Macrophages have distinct characteristics depending on their microenvironment. We performed proteomic analysis between M1 and M2 macrophages and found that cellular metabolism is the key regulator of macrophage function. We used microarray to support proteomic data between M1 and M2 macrophages. M1 macrophages are obtained using cell sorting of CD45+MHCII+CD8a-F4/80+ population from C57BL/6J bone marrow cell derived heterogenous cells under GM-CSF conditioning for 7 days. M2 macrophages are differentiated with 20% L929 cell supernatant for 7 days and sorted from CD45+F4/80+CD11b+ population.
2014-11-14 | E-GEOD-63245 | biostudies-arrayexpress
Project description:Macrophages have distinct characteristics depending on their microenvironment. We performed proteomic analysis between M1 and M2 macrophages and found that cellular metabolism is the key regulator of macrophage function. We used microarray to support proteomic data between M1 and M2 macrophages.
2014-11-14 | GSE63245 | GEO
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
Project description:Classically (M1) and alternatively activated (M2) macrophages play distinct roles in various physiological and disease processes. Understanding the gene transcription programs that contribute to macrophage polarization along the M1/M2 spectrum may lead to new tools to detect and therapeutically manipulate macrophage phenotype. Here, we define the M1 and M2 macrophage signature through mRNA microarray. The M1 macrophage signature was defined by 629 up-regulated and 732 down-regulated genes while the M2 macrophage signature was formed by 388 up-regulated and 425 down-regulated genes. While a subset of probes was common to both M1 and M2 cells, others were exclusive to each macrophage subset. The common M1/M2 pathways were characterized by changes in various transcriptional regulators and signaling partners, including increases in Kruppel-like Factor (Klf) 4, but decreases in Klf2. To identify M1 and M2 biomarkers that help discriminate these populations, we selected genes that were increased during M1 or M2 differentiation but decreased in the opposite population. Among top novel M1-distinct genes, we identified CD38, G-protein coupled receptor 18 (Gpr18) and Formyl peptide receptor 2 (Fpr2). Among top M2 genes, we found early growth response protein 2 (Egr2) and Myc. We validated these genes by Real-Time PCR and developed a CD38/Egr2-based flow cytometry assay that discriminates between M1 and M2 macrophages. Overall, this work defines the M1 and M2 signature and identifies several novel M1 and M2 genes that may be used to distinguish and manipulate M1 and M2 macrophages. Total RNA was prepared from bone marrow-derived macrophages of wild-type mice (n=2-3 independent mice) treated in M0, M1 or M2 conditions (n=2-3 replicates per condition originating from different mice)
2015-12-08 | E-GEOD-69607 | biostudies-arrayexpress
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.
2015-03-12 | GSE66805 | GEO
Project description:Classically (M1) and alternatively activated (M2) macrophages play distinct roles in various physiological and disease processes. Understanding the gene transcription programs that contribute to macrophage polarization along the M1/M2 spectrum may lead to new tools to detect and therapeutically manipulate macrophage phenotype. Here, we define the M1 and M2 macrophage signature through mRNA microarray. The M1 macrophage signature was defined by 629 up-regulated and 732 down-regulated genes while the M2 macrophage signature was formed by 388 up-regulated and 425 down-regulated genes. While a subset of probes was common to both M1 and M2 cells, others were exclusive to each macrophage subset. The common M1/M2 pathways were characterized by changes in various transcriptional regulators and signaling partners, including increases in Kruppel-like Factor (Klf) 4, but decreases in Klf2. To identify M1 and M2 biomarkers that help discriminate these populations, we selected genes that were increased during M1 or M2 differentiation but decreased in the opposite population. Among top novel M1-distinct genes, we identified CD38, G-protein coupled receptor 18 (Gpr18) and Formyl peptide receptor 2 (Fpr2). Among top M2 genes, we found early growth response protein 2 (Egr2) and Myc. We validated these genes by Real-Time PCR and developed a CD38/Egr2-based flow cytometry assay that discriminates between M1 and M2 macrophages. Overall, this work defines the M1 and M2 signature and identifies several novel M1 and M2 genes that may be used to distinguish and manipulate M1 and M2 macrophages.
2015-12-08 | GSE69607 | GEO
Project description:Purpose: Macrophages are often classified into M1 ‘classical’ and M2 ‘alternatively-activated’ macrophages. Extracellular vesicles (EVs) are biomolecule carriers involved in cell-cell communication. Here, we provide a first insight into the complete small RNA cargo of human macrophage M1/M2 EVs. Methods: Monocyte-derived macrophages were polarised into M1 (GM-CSF+LPS+IFNγ) or M2 (M-CSF+IL-4+IL-13) and EVs isolated by size exclusion chromatography. EVs were characterised by nanoparticle tracking analysis, electron microscopy and ELISA. EV RNA samples were prepared for small RNA sequencing using Qiagen’s GIAseq small RNA Library Prep kit and sequenced on an Illumina NextSeq500, single end 75 bp. Functional enrichment analysis was performed using MIENTURNET, based on validated miR-target interactions from miRTarBase. Results: Many types of small non-coding RNAs were found in EVs from M1/M2 macrophages including miRNAs, isomiRs, tRNA fragments, piRNA, snRNA, snoRNA and yRNA fragments. Distinct differences were observed between M1 and M2 EVs, with higher relative abundance of miRNAs, and lower abundance of tRNA fragments in M1 EVs compared to M2 EVs. MicroRNA-target enrichment analysis identified several gene targets involved in gene expression and metabolic processes. Conclusions: M1 and M2 cells release EVs with distinct tRNA and miRNA cargo, which have the potential to contribute to the unique effect of these cell subsets on their microenvironment.
2022-12-07 | GSE207286 | GEO
Project description:We compare M1 and M2 stimuli in human macrophages. Total RNA obtained from autologous serum monocyte-derived macrophages exposed to key cytokines, Lps, Glucocorticoid receptor ligand or left untreated.
2014-01-03 | E-GEOD-51446 | biostudies-arrayexpress
Project description:Macrophages are effector cells of the innate immune system and undergo phenotypical changes in response to organ injury and repair. They are most often classified as proinflammatory M1 and anti-inflammatory M2 macrophages. Protein arginine deiminase (PAD) enzymes, that catalyze the conversion of protein-bound arginine into citrulline, an irreversible posttranslational modification, are expressed in macrophages. However, the substrate scope of the PADs and their role in the immune cells remain not well defined. This study aims to investigate the role of PADs in the THP-1 macrophage polarization to M1 and M2 phenotype and identify the citrullinated proteins, and the modified Arg that are associated with this biological switch using mass spectrometry. Our study showed that PAD2, and to a lesser extent PAD1 and PAD4 were dominantly expressed in M1 macrophages. We showed that inhibiting PADs by BB-Cl-amidine decreased the macrophage’s polarization to M1 and increased to M2 phenotype. The process was mediated by the downregulation of proteins involved in NF-kβ pathway. Silencing of PAD2 confirmed activation to M2 macrophages through upregulation of the antiviral innate immune response and interferon signaling. 192 novel citrullination sites that belong to inflammation, cell death and DNA/RNA processing pathways were identified in M1 and M2 macrophages.
2023-03-11 | PXD034591 | Pride