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Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages

ABSTRACT: Analysis of gene expression of monocytes differentiating into macrophages in the presence of a danger signal. Kinetic analysis (1 day, 2 days, 4 days, 7 days) and analysis of lipopolysaccharide stimulated 7 day macrophages in comparison to unstimulated 7 day macrophages.

ORGANISM(S): Homo sapiens

PROVIDER: GSE180027 | GEO | 2022/01/11

REPOSITORIES: GEO

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Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages III

Project description:Purpose: We report the application of single-cell RNA sequencing for profiling the genexpression of different monocyte types in order to characterize monocytes that differentiate into macrophages under danger signal in comparison to conventional GM-CSF and M-CSF macrophages Methods: Monocytes freshly isolated from PBMCs were differentiated into GM-CSF, M-CSF, and danger-signal induced macrophages. Two million cells of each macrophage population were tagged accordingly with TotalSeq™‑B Hashtags. Single cell RNA sequencing was performed on all macrophage populations in order to characterize cells from each population. ScRNAseq analysis was performed with the R package Seurat on 16470 barcodes after filtering. Results: Cluster analysis reveals distinct separation of all three macrophage populations. Conclusion: The clear difference in overall gene expression profile suggests that macrophages exposed to danger signal differentiate into a novel macrophage type in contrast to conventional GM-CSF and M-CSF monocytes.

2022-01-11 | GSE180113 | GEO

Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages

Project description:Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages

| PRJNA746299 | ENA

Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages III

Project description:Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages III

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Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages II

Project description:Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages II

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Danger signal initiates differentiation of monocytes into osteopontin‑producing macrophages II

Project description:Analysis of gene expression of monocytes differentiating into different macrophages and dendritic cells. All cells were activated with lipopolysaccharide after differentiation.

2022-01-11 | GSE180111 | GEO

Danger signal extracellular calcium initiates differentiation of monocytes into SPP1/osteopontin-producing macrophages.

Project description:The danger signal extracellular calcium is pathophysiologically increased in the synovial fluid of patients with rheumatoid arthritis (RA). Calcium activates the NLRP3-inflammasome via the calcium-sensing receptor in monocytes/macrophages primed by lipopolysaccharide, and this effect is mediated by the uptake of calciprotein particles (CPPs) formed out of calcium, phosphate, and fetuin-A. Aim of the study was to unravel the influence of calcium on monocytes when the priming signal is not present. Monocytes were isolated from the blood of healthy controls and RA patients. Macrophages were characterized using scRNA-seq, DNA microarray, and proteomics. Imaging flow cytometry was utilized to study intracellular events. Here we show that extracellular calcium and CPPs lead to the differentiation of monocytes into calcium-macrophages when the priming signal is absent. Additional growth factors are not needed, and differentiation is triggered by calcium-dependent CPP-uptake, lysosomal alkalization due to CPP overload, and TFEB- and STAT3-dependent increased transcription of the lysosomal gene network. Calcium-macrophages have a needle-like shape, are characterized by excessive, constitutive SPP1/osteopontin production and a strong pro-inflammatory cytokine response. Calcium-macrophages differentiated out of RA monocytes show a stronger manifestation of this phenotype, suggesting the differentiation process might lead to the pro-inflammatory macrophage response seen in the RA synovial membrane.

| S-EPMC8755842 | biostudies-literature

Thrombin cleavage of osteopontin initiates osteopontin's tumor-promoting activity.

Project description:BackgroundOsteopontin (OPN) is a multifunctional proinflammatory matricellular protein overexpressed in multiple human cancers and associated with tumor progression and metastases. Thrombin cleavage of OPN reveals a cryptic binding site for α4 β1 and α9 β1 integrins.MethodsThrombin cleavage-resistant OPNR153A knock-in (OPN-KI) mice were generated and compared to OPN deficient mice (OPN-KO) and wild type (WT) mice in their ability to support growth of melanoma cells. Flow cytometry was used to analyze tumor infiltrating leukocytes.ResultsOPN-KI mice engineered with a thrombin cleavage-resistant OPN had reduced B16 melanoma growth and fewer pulmonary metastases than WT mice. The tumor suppression phenotype of the OPN-KI mouse was identical to that observed in OPN-KO mice and was replicated in WT mice by pharmacologic inhibition of thrombin with dabigatran. Tumors isolated from OPN-KI mice had increased tumor-associated macrophages with an altered activation phenotype. Immunodeficient OPN-KI mice (NOG-OPN-KI) or macrophage-depleted OPN-KI mice did not exhibit the tumor suppression phenotype. As B16 cells do not express OPN, thrombin-cleaved fragments of host OPN suppress host antitumor immune response by functionally modulating the tumor-associated macrophages. YUMM3.1 cells, which express OPN, showed less tumor suppression in the OPN-KI and OPN-KO mice than B16 cells, but its growth was suppressed by dabigatran similar to B16 cells.ConclusionsThrombin cleavage of OPN, derived from the host and the tumor, initiates OPN's tumor-promoting activity in vivo.

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Lipid droplet-mediated danger signaling balances Trem2+ macrophage induction and NLRP3 inflammasome activation in NASH

Project description:Macrophages are exquisitely capable of sensing danger-associated molecular patterns (DAMPs) and orchestrating inflammatory response during tissue injury. Nonalcoholic steatohepatitis (NASH) represents an advanced stage of metabolic fatty liver disease that increases the risk for cirrhosis and liver cancer. Pathogenic mechanisms of NASH center on hepatocyte injury and the ensuing immune response within the liver microenvironment. However, the nature of DAMPs released by injured hepatocytes and how they shape the liver immune milieu remain largely unknown. Here we show that lipid droplets (LDs) released by injured fatty hepatocytes provide a potent signal that triggers monocyte infiltration and maturation into Trem2+ macrophages, recently described as NASH-associated macrophages (NAMs) or lipid- associated macrophages. LD treatment exacerbated liver injury in mice with diet-induced NASH. We identified Membrane spanning 4-domains a7 (Ms4a7) as a NAM-specific pathogenic factor that was strongly induced in mouse and human NASH. Ms4a7 inactivation ameliorated key aspects of diet-induced NASH pathologies in mice. At the mechanistic level, Ms4a7 physically interacts with NLR family pyrin domain containing 3 (NLRP3) and is required for endosomal NLRP3 inflammasome activation. These findings illustrate a crucial role of Ms4a7 in driving pro-inflammatory signaling in NASH liver. Surprisingly, LD treatments attenuated Ms4a7 expression and NLRP3 inflammasome activation in cultured macrophages. As such, LDs serve as a DAMP signal that balances the induction of Trem2+ macrophages and NLRP3 inflammasome activation in NASH liver

2024-04-26 | GSE230700 | GEO

Danger signals activate the innate immune system of a filamentous fungus during regeneration

Project description:The ability to respond to injury is a biological process conserved across kingdoms, which in some cases results in regeneration of an organism’s lost part or structure. Due to their immobility, multicellular fungi are prey to a variety of predators and are therefore constantly exposed to mechanical damage. Nevertheless, our current knowledge of how fungi respond to injury is scarce. Activation of injury responses and regeneration relies on the detection of danger or alarm signals known as Danger- or Damage-Associated Molecular Patterns. We show that Ca2+ influxes and extracellular ATP, two such signals, together with Mitogen-Activated Protein Kinases, play a key role in the control of hyphal regeneration in the filamentous fungus Trichoderma atroviride. We further show that these signaling cascades activate major transcriptional changes early after injury. We identified a set of regeneration genes related to cell signaling, stress responses, regulation of transcription, ribosome biogenesis/translation, replication and DNA repair. We uncovered the activation of an innate immune response, including HET domain genes, until now only known to participate in vegetative incompatibility. We show that fungal and animal regeneration share danger-signals, signaling cascades, and the activation of an immune system, challenging the current notion of the evolution of this process.

2018-08-14 | GSE115811 | GEO

To determine the global gene expression response in murine LPS-induced macrophages treated with a bromodomain inhibitor.

Project description:Bone marrow-derived macrophages, Unstimulated DMSO Bone marrow-derived macrophages, Unstimulated + I-BET (GSK525762A) Bone marrow-derived macrophages, LPS 1h DMSO Bone marrow-derived macrophages, LPS 1h + I-BET (GSK525762A) Bone marrow-derived macrophages, LPS 2h DMSO Bone marrow-derived macrophages, LPS 2h + I-BET (GSK525762A) Bone marrow-derived macrophages, LPS 4h DMSO Bone marrow-derived macrophages, LPS 4h + I-BET (GSK525762A) LPS (100 ng/mL) was purchased from Sigma. Bone Marrow-derived macrophages (BMDMs) were differentiated from C57BL/6 bone marrow using 5 ng/mL each of recombinant M-CSF and IL-3 (Peprotech) for 7 days as described (Jeffrey et al, Nature Immunology, 2006). 2 x10^6 BMDMs were treated with DMSO or 1 μM of I-BET for 30 minutes before the addition of LPS (100 ng/mL) for 1, 2 or 4h. Unstimulated control samples were incubated with I-BET only for 1 hour. 500 ng of total RNA from 3 independent samples per group was used to prepare biotin-labeled RNA using Ambion Illumina TotalPrep RNA Amplification Kit (Applied Biosystems) and hybridized to Illumina MouseRef-8 v2.0 expression BeadChip kits. The chips were scanned using Illumina BeadArray Reader.

2010-11-10 | GSE21764 | GEO

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