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Change in gene expression following CSF1 stimulation of mouse cancer prostate cell lines overexpressing the c-fms receptor.

ABSTRACT: To study the role of the c-fms tyrosine kinase receptor expression in prostate cancer cells, we generated a cell line model from the C2H mouse prostate cancer cell line overexpressing the c-fms receptor (N18-CFMS clone) and treated it or not with the c-fms ligand CSF1.

ORGANISM(S): Mus musculus

PROVIDER: GSE216628 | GEO | 2022/12/09

REPOSITORIES: GEO

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Change in gene expression following CSF1 stimulation of mouse cancer prostate cell lines overexpressing the c-fms receptor.

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Project description:Caspases, which are key effectors of apoptosis, have demonstrated non-apoptotic functions. One of these functions is the differentiation into macrophages of peripheral blood monocytes exposed to Colony-Stimulating Factor-1 (CSF1). Macrophage polarization plays an important role in the pathogenesis of diverse human diseases as cancer, leading us to explore if caspase inhibition would affect macrophage polarization. To explore the role of caspases in CSF1 differentiation, we used human monocytes sorted from buffy coats treated by cytokines. We reported that caspase inhibition delays the ex vivo differentiation of peripheral blood monocytes exposed to CSF1 and modifies the phenotype of generated macrophages, e.g. cell shape, surface markers. Moreover, by RNAseq, we observed that the macrophages generated in presence of CSF1 and QVD are different from CSF1-treated monocytes. This study confirms the importance of caspase activation in CSF1 differentiation.

2024-01-01 | E-MTAB-8088 | biostudies-arrayexpress

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Project description:Caspases, which are key effectors of apoptosis, have demonstrated non-apoptotic functions. One of these functions is the differentiation into macrophages of peripheral blood monocytes exposed to Colony-Stimulating Factor-1 (CSF1). Conversely, GM-CSF induces the differentiation of monocytes into macrophages in a caspase-independent manner. Macrophages generated by CSF1 and GM-CSF have distinct polarity. Macrophage polarization plays an important role in the pathogenesis of diverse human diseases as cancer, leading us to explore if caspase inhibition would affect macrophage polarization. To explore the role of caspases in CSF1 differentiation, we used human monocytes sorted from buffy coats treated by cytokines. We reported that caspase inhibition delays the ex vivo differentiation of peripheral blood monocytes exposed to CSF1 and modifies the phenotype of generated macrophages, e.g. cell shape, surface markers. Moreover, by RNAseq, we observed that the macrophages generated in presence of CSF1 and QVD are different from CSF1-treated monocytes and from GM-CSF-treated monocytes. Cell cycle and focal adhesion-related pathway genes were selectively down-regulated. This study confirms the importance of caspase activation in CSF1 differentiation.

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Microglial responses to CSF1 overexpression do not promote expansion of other glial lineages

Project description:CSF1 expression in the central nervous system (CNS) increases in response to a variety of stimuli, and CSF1 is overexpressed in many CNS diseases. In young adult mice we previously showed that CSF1 overexpression in the CNS caused proliferation of IBA1+ microglia without promoting expression of M2 polarization markers. Here we further examine the impacts of increased CSF1 levels in the brain. As CSF1 over-expressing mice age, IBA1+ cell numbers are constrained by a decline in proliferation rate. Compared to controls, there were no differences in expression of the M2 markers ARG1 and MRC1 (CD206) in CSF1 overexpressing mice of any age, indicating that even prolonged exposure to increased CSF1 is not sufficient to promote M2 polarization in vivo. Moreover, RNA-sequencing (RNA-seq) confirmed the lack of increased expression of markers of M2 polarization in microglia exposed to CSF1 over-expression, but did reveal changes in expression of other immune related genes. Although treatment with inhibitors of the CSF1 receptor, CSF1R, has been shown to impact other glia, no increased expression of astrocyte or oligodendrocyte lineage markers was observed in CSF1 OE mice. Our data indicate that CSF1 overexpression as an isolated stimulus has limited impacts in the CNS, and that microglia ultimately adapt to the presence of the CSF1 mitogenic signal.

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Project description:The expression was designed to determine whether exposure to CSF1-Fc has any effect on liver-specific gene expression in pigs. livers from pigs exposed to CSF1-Fc

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Expression data from CSF1- or CSF2-induced bone marrow derived macrophages (BMDMs): M(CSF1) and M(CSF2) cells.

Project description:Femur and tibia bones were harvested from 8-week-old wild-type (WT) C57BL/6 mice. Bone marrow was flushed out into cold PBS (Life Technologies) plus 2% heat-inactivated FBS, passed through a needle five times to dissociate the cells, and then passed through a 70-μm cell strainer (Becton Dickinson) to remove cell clumps, bone, hair, and other cells/tissues. After addition of three volumes of NH4Cl solution (0.8% NH4Cl solution; Beyotime Institute of Biotechnology, Jiangsu, China), the mixture was incubated on ice for 10 min to remove red blood cells; the cells were then spun down and resuspended in cold PBS with 2% FBS. The harvested cells were cultured in DMEM containing 10% FBS and supplemented with 10 ng/ml recombinant mouse CSF1 (R&D Systems) or 10 ng/ml recombinant mouse CSF2 (R&D Systems) for 7 days to obtain CSF1- or CSF2-induced BMDMs: M(CSF1) or M(CSF2) cells, respectively. To test the difference genes expression of TAMs obtained from M(CSF1) and M(CSF2) cells in C57BL/6 mice. We used microarrays to detail the global programme of gene expression and identified M(CSF1) and M(CSF2) cells during this process.

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