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Mus musculus

ABSTRACT: High throughput quantitative whole transcriptome analysis of individual macrophages 7 days post-pneumonectomy in a B6 CSF1R-GFP mouse

PROVIDER: PRJNA378847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5336930_1.fastq.gz	Fastqsanger.gz
	SRR5336930_2.fastq.gz	Fastqsanger.gz
	SRR5336940_1.fastq.gz	Fastqsanger.gz
	SRR5336940_2.fastq.gz	Fastqsanger.gz
	SRR5336950_1.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:High throughput quantitative whole transcriptome analysis of individual macrophages 7 days post-sham thoracotomy in B6 CSF1R-GFP mice

| PRJNA378846 | ENA

High throughput quantitative whole transcriptome analysis of individual macrophages 7 days post-pneumonectomy in a B6 CSF1R-GFP mouse

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

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Project description:The medial and cardiac lobes of the right lung and whole right lung of (initially) 10-12 week old C57BL/6 mice were transcriptome profiled at days 0, 3, 7, 14, 28 and 56 post left pneumonectomy, with day 0 being pre-pneumonectomy, and an additional day 56 post sham surgery to control for 8 week aging post left pneumonectomy. pneumonectomy time course

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Identification of de-differentiation and re-development phases during post-pneumonectomy lung growth.

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High throughput quantitative whole transcriptome analysis of individual macrophages 7 days post-sham thoracotomy in B6 CSF1R-GFP mice

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.

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Effect of CSF1R inhibition in tumor macrophages on gene expression in metastatic epithelial cells

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.

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Project description:Microglia, the brain's resident macrophages, depend on interleukin 34 (IL-34) and colony-stimulating factor 1 (CSF1) for their development and maintenance, engaging the CSF1 receptor (CSF1R). Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP), a neurodegenerative disorder affecting the brain's white matter, is caused by heterozygous pathogenic mutations in the CSF1R gene. Neuropathological studies of postmortem ALSP brains have shown widespread depletion of microglia, demyelination of cerebral white matter, axonal swellings, and pigmented glial cells. In this study, we investigated how individual brain cell populations respond to microglia depletion and contribute to ALSP progression. To do this, we analyzed post-mortem specimens from patients wirth ALSP using single-nucleus RNA-seq (snRNA-seq).

2025-08-13 | GSE295854 | GEO

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