Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-60528
PROVIDER: PRJNA258470 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mouse GM-CSF-related alveolar macrophage genome-wide expression data
2015-07-29 | E-GEOD-60528 | ExpressionAtlas
Project description:Pulmonary conventional dendritic cells (cDCs) are functionally and phenotypically heterogeneous antigen-presenting cells essential for orchestrating adaptive immune responses in the lung. Here, we define a critical role for granulocyte-macrophage colony-stimulating factor (GM-CSF) in generating a CD301b+ subset of terminally differentiated cDC2s. GM-CSF signaling is intrinsically required for their development, independent of GM-CSF-dependent alveolar macrophages. Absence of GM-CSF results in a defect similar to that seen in CD103+XCR1+ cDC1s. Unbiased single-cell transcriptomic profiling of CD11c+ cells identified both immature and differentiated cDC populations. GM-CSF deficiency disrupted anti-apoptotic Bcl2a1 upregulation and impaired progression to the CD301b+ transcriptional state. Despite their positioning in lymphoid cell-rich adventitial cuff areas, hematopoietic GM-CSF was dispensable. Instead, genetic GM-CSF gain- and loss-of-function studies showed that alveolar epithelial type 2 cell-derived GM-CSF is required for CD301b+ cDC2 formation and pulmonary type 2 immune responses, highlighting the central role of GM-CSF signaling in shaping the pulmonary myeloid landscape.
2025-08-04 | GSE295575 | GEO
Project description:Lung-specific expression of the SOCS family member Cish is driven by steady-state GM-CSF signaling and shapes alveolar macrophage identity and homeostatic function.
2021-08-26 | GSE156967 | GEO
Project description:<p>Macrophages play a critical role in the inflammatory response and tumor development. Macrophages are primarily divided into pro-inflammatory M1-like and anti-inflammatory M2-like macrophages based on their activation status and functions. <em>In vitro</em> macrophage models could be derived from mouse bone marrow cells stimulated with two types of differentiation factors: GM-CSF (GM-BMDMs) and M-CSF (M-BMDMs), to represent M1-and M2-like macrophages, respectively. Since macrophage differentiation requires coordinated metabolic reprogramming and transcriptional rewiring in order to fulfill their distinct roles, we combined both transcriptome and metabolome analysis, coupled with experimental validation, to gain insight into the metabolic status of GM-and M-BMDMs. The data revealed higher levels of the tricarboxylic acid cycle (TCA cycle), oxidative phosphorylation (OXPHOS), fatty acid oxidation (FAO), and urea and ornithine production from arginine in GM-BMDMs, and a preference for glycolysis, fatty acid storage, bile acid metabolism, and citrulline and nitric oxide (NO) production from arginine in M-BMDMs. Correlation analysis with the proteomic data showed high consistency in the mRNA and protein levels of metabolic genes. Similar results were also obtained when compared to RNA-seq data of human monocyte derived macrophages from the GEO database. Furthermore, canonical macrophage functions such as inflammatory response and phagocytosis were tightly associated with the representative metabolic pathways. In the current study, we identified the core metabolites, metabolic genes, and functional terms of the two distinct mouse macrophage populations. We also distinguished the metabolic influences of the differentiation factors GM-CSF and M-CSF, and wish to provide valuable information for <em>in vitro</em> macrophage studies. </p>
2023-09-19 | MTBLS6502 | MetaboLights
Project description:A genome wide microarray identified 19 candidate miRNA altered in primary AEC during oxidative stress with reversal by treatment with GM-CSF. Three of these microRNA (miR 133a, miR133a* and miR133b) are also predicited to bind the GM-CSF 3 UTR. 4 samples. Primary murine alveolar epithelial cells were isolated and subjected to room air or 80% oxygen in the presence or absence of recombinant murine GM-CSF (20 ng/ml). Total RNA was extracted and quality checked (260/280>2 and 260/230 > 1.6). Mouse genome microRNA analysis (MAM3200) was performed by SABioscience.
2014-04-11 | E-GEOD-56687 | biostudies-arrayexpress
Project description:To explore reovirus-macrophage interactions, we performed tandem mass tag (TMT)-based quantitative temporal proteomics on mouse bone marrow-derived macrophages (BMMs) generated with 2 cytokines, M-CSF and GM-CSF, representing anti- and pro-inflammatory macrophages, respectively. We quantified 6,863 proteins across five time points in duplicate, comparing M-CSF (M-BMM) and GM-CSF (GM-BMM) in response to OV. We find that GM-BMMs have lower expression of key intrinsic proteins that facilitate an anti-viral immune response, express higher levels of reovirus receptor protein JAM-A and are more susceptible to oncolytic reovirus infection compared to M-BMMs. Interestingly, although M-BMMs are less susceptible to reovirus infection and subsequent cell death, they initiate an anti-reovirus adaptive T cell immune response comparable to that of GM-BMMs. Taken together, these data describe distinct proteome differences between these two macrophage populations in terms of their ability to mount anti-viral immune responses.
2020-01-07 | PXD015203 | Pride
Project description:The functional versatility of macrophages is intrincately tied to factors such as their ontogeny and the specific tissue and extracellular environment. Monocyte-derived macrophages are oppositely instructed by M-CSF or GM-CSF. GM-CSF drives monocyte-derived macrophages towards heightened pro-inflammatory activity and the acquisition of the lung alveolar macrophage phenotype and gene profile whereas M-CSF gives rise to anti-inflammatory, pro-resolving, and immunosuppressive monocyte-derived macrophages. We explored the molecular impact of blocking GSK3 on the gene expression profile in GM-CSF-primed human monocyte derived macrophages. GSK3 inhibition skewed the transcriptional profile of GM-MØ towards an anti-inflammatory phenotype.
2025-04-16 | GSE256208 | GEO
Project description:GM-CSF receptor-β deficient (Csf2rbâ/â or KO) mice develop a lung disease identical to hereditary pulmonary alveolar proteinosis (hPAP) in humans with recessive CSF2RA or CSF2RB mutations that impair GM-CSF receptor function. We performed pulmonary macrophage transplantation (PMT) of bone marrow derived macrophages (BMDMs) without myeloablation in Csf2rbâ/âmice. BMDMs were administered by endotracheal instillation into 2 month-old Csf2rbâ/â mice. Results demonstrated that PMT therapeutic of hPAP in Csf2rbâ/â mice was highly efficacious and durable. Alveolar macrophages were isolated by bronchoalveolar lavage one year after administration subjected to microarray analysis to determine the effects of PMT therapy on the global gene expression profile. Total mRNA was isolated from alveolar macrophages PMT-treated Csf2rbâ/âmice (PMT) and from age-matched, untreated KO mice (KO) and wild-type (C57Bl/6) mice (WT). Total mRNA was evaluated using Affymetrix microarrays (Mouse Gene 1.0 ST Array) to compare the gene expression profiles among the three groups (3 mice/group).
2014-10-01 | E-GEOD-60528 | biostudies-arrayexpress
Project description:The functional versatility of macrophages is intrincately tied to factors such as their ontogeny and the specific tissue and extracellular environment. Monocyte-derived macrophages are oppositely instructed by M-CSF or GM-CSF. GM-CSF drives monocyte-derived macrophages towards heightened pro-inflammatory activity and the acquisition of the lung alveolar macrophage phenotype and gene profile whereas M-CSF gives rise to anti-inflammatory, pro-resolving, and immunosuppressive monocyte-derived macrophages. We explored the molecular impact of siRNA mediated knocking-down GSK3A, GSK3B or both (GSK3A/B) on the gene expression profile of GM-CSF-primed human monocyte derived macrophages. GSK3A/B knowdown skewed the transcriptional profile of GM-MØ towards an anti-inflammatory phenotype.
2025-04-16 | GSE266236 | GEO
Project description:Systemic GM-CSF promotes myelopoiesis and inflammation and GM-CSF blockade is being evaluated as treatment for COVID-19-associated hyperinflammation. Alveolar GM-CSF is however required for monocytes to differentiate into alveolar macrophages (AM) that control alveolar homeostasis and dampen inflammation. By mapping cross-species AM development stages to clinical lung samples, we discovered that COVID-19 is marked by defective GM-CSF-dependent AM instruction and accumulation of proinflammatory macrophages. In a multi-center, open-label, randomized, controlled trial in 81 non-ventilated COVID-19 patients with respiratory failure, we found that inhalation of rhu-GM-CSF did not improve mean oxygenation parameters compared with standard treatment. However, more patients on GM-CSF had a clinical response, and GM-CSF inhalation induced higher numbers of virus-specific CD8 effector lymphocytes and class-switched B cells, without exacerbating systemic hyperinflammation. This translational proof-of-concept study provides rationale for further testing of inhaled GM-CSF as non-invasive treatment to improve alveolar gas exchange and simultaneously boost anti-viral immunity in COVID-19
2022-11-03 | GSE216704 | GEO