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Integrated analysis of long non-coding RNAs expression profiles in THP-1 induced M0, M1 and M2 macrophage and GCC culture medium induced similar M2 (CM-sM2)

ABSTRACT: We used microarray and bioinformatics analysis to find potential lncRNAs which may be useful in the polarization of macrophages

ORGANISM(S): Homo sapiens

PROVIDER: GSE146895 | GEO | 2022/03/12

REPOSITORIES: GEO

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Glycoproteomics of human THP-1-derived M0, M1 and M2 macrophages

Project description:In this study, we used human THP-1-derived macrophages as an immune cell model, and systematically performed glycoproteomics of three subtypes of macrophages by StrucGP.To study the N‑Glycoproteomic of them, the intact glycopeptides were first enriched and identified using triplicate mass spectrometry (MS)-based glycoproteomic approaches, then StrucGP was used for subsequent analysis. In total three subtypes of macrophages, these intact glycopeptides consist of 253 N-linked glycan structures at 652 unique glycosites from 372 N-glycoproteins, along with their PSM information. A total of 135, 163, and 201 N-glycan structures were identified from M0, M1, and M2 macrophages, respectively.

2023-10-19 | PXD030277 | Pride

Differentially polarized human monocyte-derived macrophages (M0, M1, M2/IL10, M2/IL4, TAM-like)

Project description:In order to assess whether differences in the transcriptomic profile of human tumor-associated macrophages vs. alveolar macrophages from adjacent non-tumor-tissue (GSE162669) were caused by factors secreted by tumor cells, primary human monocyte-derived macrophages (MDMs) were polarized towards a TAM-like phenotype by cultivating them in tumor cell-conditioned medium. A genome-wide comparison by bulk RNA-Seq confirmed a high similarity of ex vivo TAMs and in vitro polarized TAM-like macrophages. Other polarization schemes (M1: LPS/IFN-gamma, M2: IL10 or IL4) did not lead to similar transcriptomic changes. For details, see Hoppstädter et al., 2021 (doi:10.1016/j.ebiom.2021.103578).

2021-09-25 | GSE162698 | GEO

Integrated analysis of long non-coding RNAs expression profiles in THP-1 induced M0, M1 and M2 macrophage and GCC culture medium induced similar M2 (CM-sM2)

Project description:Integrated analysis of long non-coding RNAs expression profiles in THP-1 induced M0, M1 and M2 macrophage and GCC culture medium induced similar M2 (CM-sM2)

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Expression analysis of microRNAs in INT-HA-induced M2-like macrophages and untreated macrophages (M0)

Project description:Using the highly sensitive miRNA microarray, we screened 107 up-regulated microRNAs and 33 down-regulated microRNAs in the INT-HA-induced M2-like macrophages and we explored the functions of these miRNAs in macrophage polarization. The enrichment results indicated that these miRNAs might participate in the process of macrophage polarization. Furthermore, the quantitative real-time polymerase chain reaction results showed that miR-935 may play an important role in M2 macrophage polarization which was activated by INT-HA.

2021-02-08 | GSE110339 | GEO

Proteomics of THP-1 macrophages polarization to M1 and M2 phenotype and treated with BB-Cl-amidine

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.

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Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice.

Project description:Obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell–like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization. 15 samples; 2 genotypes and 2 time points

2012-03-22 | E-GEOD-36669 | biostudies-arrayexpress

Exosomes derived from M0, M1 and M2 macrophages exert distinct influences on the proliferation and differentiation of mesenchymal stem cells.

Project description: Not available

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Microarray of non-polarized and M1- and M2-polarized canine macrophages in vitro

Project description:Unstimulated (M0), M1-polarized (GM-CSF, LPS, IFNÎ³-stimulated), and M2-polarized (M-CSF, IL-4-stimulated) canine blood-derived macrophages were generated in vitro and investigated for differences in their transcriptome to create a basis for future investigations upon the role of macrophage polarization in dogs, a species, which has emerging importance for translational research.

2017-08-10 | E-MTAB-5458 | biostudies-arrayexpress

Gene expression profiles of the M1/M2 polarized Kupffer cells

Project description:To reveal the transcriptomes associated with M1 or M2-polarized Kupffer cells, the primary Kupffer cells isolated from mouse liver were treated with lipopolysaccharides or IL-4 and the gene expression patterns were analyzed by microarray. To study the role of RORα in Kupffer cell polarization, Kupffer cells were treated with RORα ligands and transcriptions were compared with those of the M1/M2 polarized Kupffer cells.

2016-09-03 | GSE86397 | GEO

Transcriptomic analysis of monocytes, M0, M1 and M2 macropahges from H syndrome patients and SAIDs.

Project description:Biallelic mutations in SLC29A3 cause histiocytosis-lymphadenopathy plus syndrome, also known as H syndrome (HS). HS is a complex disorder, with ~25% of patients developing autoinflammatory complications consisting of unexplained fevers, persistently elevated inflammatory markers and unusual lymphadenopathies, with infiltrating CD68+, S100+ and CD1a– histiocytes, resembling the immunophenotype found in Rosai-Dorfman disease (RDD). We investigated the transcriptomic profiles of monocytes, non-activated (M0), classically-activated (M1) and alternatively-activated macrophages (M2) in two patients with HS, one without autoinflammatory (HS1) and one with autoinflammatory complications (HS2). RNA sequencing revealed a dysregulated transcriptomic profile in both HS patients compared to healthy controls (HC). HS2, when compared to HS1, had several differentially expressed genes, including genes associated with lymphocytic-histiocytic predominance (e.g. NINL) and immunodeficiencies (e.g. B2M). The transcriptomic and cytokine profiles of HS patients were comparable to patients with SAID with high levels of TNF. SERPINA1 gene expression was found to be upregulated in all patients. Moreover, higher levels of IFNg were found in the serum of both HS patients when compared to HC. Gene-ontology (GO) enrichment analysis of the DEGs in HS patients revealed the terms "type I IFN", "IFNg signalling pathway" and "immune responses" as the top 3 most significant terms for monocytes. Finally, the transcriptomic profiles of M0 and M1 macrophages, from patient HS2, were similar to the transcriptomic profile of tissue biopsies taken from patients with RDD-like lymphadenopathies. Monocytes and macrophages from both HS patients showed transcriptomic profiles similar to SAIDs and with a unique dysregulated IFNgsignalling. These findings may help to find better therapeutic options for this rare disorder.

2021-02-16 | GSE155697 | GEO

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