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RNAseq of untreated, CSF1-treated, CSF1+QVD-treated, and GM-CSF-treated monocytes

ABSTRACT: 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.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER: STEPHANIE SOLIER

PROVIDER: E-MTAB-5752 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RNAseq of untreated and CSF1-treated, CSF1+QVD-treated monocytes

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

RNAseq of untreated, CSF1-treated, CSF1+QVD-treated, and GM-CSF-treated monocytes

Project description:RNAseq of untreated, CSF1-treated, CSF1+QVD-treated, and GM-CSF-treated monocytes

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Differentiation of human monocytes to macrophages in the presence of GM-CSF +/- forskolin (FSK)

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Comparison of the DNA methylation profiles of CD14+ monocytes from human peripheral blood with DCs and MACs obtained by exposure with GM-CSF/IL-4 and GM-CSF, respectively, and with mature DCs and MACs after LPS exposure

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2015-12-11 | E-GEOD-71837 | biostudies-arrayexpress

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2015-12-12 | E-GEOD-75937 | biostudies-arrayexpress

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2010-06-16 | E-GEOD-19236 | biostudies-arrayexpress

Differentiation of human monocytes to macrophages in the presence of GM-CSF +/- forskolin (FSK)

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Simultaneous inhibition of PPAR-γ and mTORC1 enables GM-CSF to induce the differentiation of monocytes into highly immunogenic dendritic cells

Project description:Monocytes can differentiate into macrophages or dendritic cells. When treated with granulocyte-macrophage colony-stimulating factor (GM-CSF) monocytes differentiate into macrophage-like cells. Here, we report that pharmacological blockade of the nuclear receptor PPARγ in monocytes turns GM-CSF into a potent inducer of dendritic cell (Mo-DC) differentiation. Remarkably, simultaneous blockade of PPARγ and mTORC1 in the presence of GM-CSF promoted the differentiation of Mo-DCs with a stronger phenotypic stability and immunogenic profile when compared with canonical Mo-DCs differentiated by treatment with GM-CSF and IL-4. Moreover, and in contrast with the observations made with GM-CSF and IL-4, blockade of PPARγ and mTORC1 was shown to be able to induce the differentiation of monocyte-derived macrophages (Mo-Macs) into Mo-DCs. Transcriptional profiling performed at either early time points, as well as at the end of the differentiation process, revealed marked differences in the gene expression signature between Mo-DCs induced by GM-CSF and IL-4 and Mo-DCs induced by GM-CSF in the presence of PPARγ and/or mTORC1 inhibitors, thus suggesting diverging differentiation pathways. Our observations might contribute, not only to a better understanding of the mechanisms involved in Mo-DCs differentiation but also to improving the efficacy of both, DC vaccines and therapies focusing on the modulation of myeloid cell functions.

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