Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA378847 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:High throughput quantitative whole transcriptome analysis of individual macrophages 7 days post-sham thoracotomy in B6 CSF1R-GFP mice
| PRJNA378846 | ENA
Project description:To define the mechanisms that underlie regeneration driven by EP4+ macrophages, we transcriptionally compared the WT and Csf1r-EP4-/- mature macrophages isolated from colon by 39 days post DSS treatment.
2019-11-28 | GSE141093 | GEO
Project description:Metastasis is the primary cause of mortality in breast cancer patients. Tumor associated macrophages (TAMs) are active collaborators in mediating several steps of the tumor metastatic cascade, but the molecular details governing this collaboration remain ill-defined. Colony Stimulating Factor 1 (CSF1), a factor critical for macrophage differentiation and survival, functions to recruit TAMs to the primary tumor site, and anti-CSF1 therapies are in clinical trials.In this study, we tested the effect of inhibiting CSF1 signaling in macrophages on gene expression in metastatic tumor cells in mouse models of breast cancer metastasis. Tumor cells were sorted from lung metastases from control and CSF1R inhibitor treated mice. Several pro-tumor processes were significantly affected by CSF1R inhibitor treatment, including angiogenesis and tumor cell proliferation. In addition, a 29 gene signature derived from this data could retrospectively predict survival in a cohort of luminal B breast cancer patients. Collectievly, our results highlight the utility of employing CSF1R inhibitors for the treatment of metastatic breast cancer. GFP tagged MVT1 metastatic mammary tumor cells were injected intravenously into FVB/N mice. Mice were gavaged with the CSF1R inhibitor GW2580 or vehicle starting one week post injection. GFP tagged tumor cells were sorted from metastatic tumor bearing lungs 1 and 2 weeks post injection from 2 vehicle treated mice for each. These are denoted 1_week_WT and 2_week_WT respectively. GFP tagged tumor cells were simultaneously sorted from mice gavaged with GW2580. These samples are denoted 2_week_GW. RNA was extracted and gene expression profiling was performed using the Affymetrix Mouse Genome 430 2.0 Array platform.
2014-03-13 | E-GEOD-55855 | biostudies-arrayexpress
Project description:Using fluorescence activated cell sorting, we isolated CD45+, CSF1R-GFP+, F4/80+, Ly6G- mouse lung monocytes and macrophages at 7 days after sham thoracotomy procedures. We then used microfluidic single cell RNA-sequencing to transcriptional profile unique myeloid subsets.
2017-06-19 | GSE96105 | GEO
Project description:Using fluorescence activated cell sorting, we isolated CD45+, CSF1R-GFP+, F4/80+, Ly6G- mouse lung monocytes and macrophages at 7 days after pneumonectomy procedure. We then used microfluidic single cell RNA-sequencing to transcriptional profile unique myeloid subsets. Using the pneumonectomy dataset, we identified 6 cell groups and 4 gene groups that marked several regenerative macrophage subsets including CCR2+, Ly6C+ monocytes and CD206+, Chil3+ M2-like macrophages.
2017-06-19 | GSE96104 | GEO
Project description:We performed a genome binding/occupancy profiling by high throughput sequencing (ChIP-seq) of root meristems of 3 days post germination old transgenic lines expressing GFP-tagged ARR12 (ARR12-GFP) as well as Col-0 as negative control to identify ARR12 direct target genes.
2020-05-20 | GSE134695 | GEO
Project description:Cardiac macrophages exhibit remarkable heterogeneity that is accentuated after myocardial infarction. In order to characterize the transcriptional profile of cardiac macrophage subpopulations after infarction we performed scRNA-seq in FACS-sorted macrophages from normal and infarcted CSF1R-EGFP (macrophage reporter) mouse hearts. CSF1R-EGFP 12-16 week-old mice were subjected to permanent coronary occlusion, and 7 days after surgery macrophage suspensions were harvested from infarcted and control mice. Non-neutrophils (Ly6G-) were gated to identify EGFP+ macrophages, which were sorted with the FACSAria Sorter (BD Biosciences). Subsequently, scRNA-seq was performed.
2023-11-03 | GSE227251 | GEO
Project description:We used zebrafish lacking functional csf1r to unravel how and when csf1r is necessary for the development of early tissue macrophages from embryonic macrophages. Transcriptomic analysis of mpeg+ macrophages revealed that csf1r deficient macrophages show a macrophage transcriptome, but reduced expression of cell cycle and RNA/DNA metabolism related genes. Transcriptional changes over time were similar between wildtype controls als csf1r deficient embryonic macrophages.
2020-05-05 | GSE149786 | GEO
Project description:Chronic graft-versus-host disease (cGVHD) remains a significant complication of allogeneic hematopoietic stem cell transplantation. Central nervous system (CNS) involvement is becoming increasingly recognised, where brain-infiltrating donor MHC class II+ bone marrow-derived macrophages (BMDM) drive pathology. BMDM are also mediators of cutaneous and pulmonary cGVHD, and clinical trials assessing the efficacy of antibody blockade of colony-stimulating factor 1 receptor (CSF1R) to deplete macrophages are promising. We hypothesised that CSF1R antibody blockade may also be a useful strategy to prevent/treat CNS cGVHD. Increased blood-brain barrier permeability during acute GVHD (aGVHD) facilitated CNS antibody access and microglia depletion by anti-CSF1R treatment. However, CSF1R blockade early post-transplant unexpectedly exacerbated aGVHD neuroinflammation. In established cGVHD, vascular changes and anti-CSF1R efficacy were more limited. Anti-CSF1R-treated mice retained donor BMDM, activated microglia, CD8+ and CD4+ T cells, and local cytokine expression in the brain. These findings were recapitulated in GVHD recipients where CSF1R was conditionally depleted in donor CX3CR1+ BMDM. Notably, inhibition of CSF1R signalling post-transplant failed to reverse GVHD-induced behavioural changes. Moreover, we observed aberrant behaviour in non-GVHD control recipients administered anti-CSF1R blocking antibody and naïve mice lacking CSF1R in CX3CR1+ cells, revealing a novel role for homeostatic microglia and indicating that ongoing clinical trials of CSF1R inhibition should assess neurological adverse events in patients. In contrast, transfer of Ifngr-/- grafts could reduce MHC class II+ BMDM infiltration, resulting in improved neurocognitive function. Our findings highlight unexpected neurological immune toxicity during CSF1R blockade and provide alternative targets for the treatment of cGVHD within the CNS.
2023-10-18 | GSE245360 | GEO
Project description:Normal arteries contain a large population of tissue resident macrophages (MΦ). Their origins, as well as the mechanisms that sustain them during homeostasis and disease, however, are poorly understood. Gene expression profiling, we show, identifies arterial MΦ as a distinct population among tissue MΦ. Ontologically, arterial MΦ arise before birth, though CX3CR1-, Csf1r-, and Flt3-driven fate mapping approaches demonstrate MΦ colonization occurs through successive contributions of yolk sac (YS) and conventional hematopoiesis. In adulthood, arterial MΦ renewal is driven by local proliferation rather than monocyte recruitment from the blood. Proliferation sustains MΦ not only during steady state conditions, but mediates their rebound after severe depletion following sepsis. Importantly, the return of arterial MΦ to functional homeostasis after infection is rapid; repopulated MΦ exhibit a transcriptional program similar to resting MΦ and efficiently phagocytose bacteria. Collectively, our data provide a detailed framework for future studies of arterial MΦ function in health and disease. Aortic macrophages (CD11bhighF4/80highCD45+MerTK+CD64+) were isolated from C57/B6 wild-type male mice aged 6-8 weeks before and 7 days after induction of sepsis by cecal puncture. 18-20 aortas were pooled per sample. Each condition contained three biological replicates.
2015-12-07 | E-GEOD-68968 | biostudies-arrayexpress