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Genome-wide identification of H3K27ac & H3K4me3-binding sequences upon LPS & CSF1 stimuli in mouse oocytes

ABSTRACT: Genome-wide identification of H3K27ac & H3K4me3-binding sequences upon LPS & CSF1 stimuli in mouse oocytes

PROVIDER: PRJNA790838 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17278655_1.fastq.gz	Fastqsanger.gz
	SRR17278655_2.fastq.gz	Fastqsanger.gz
	SRR17278656_1.fastq.gz	Fastqsanger.gz
	SRR17278656_2.fastq.gz	Fastqsanger.gz
	SRR17278657_1.fastq.gz	Fastqsanger.gz

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Genome-wide identification of H3K27ac & H3K4me3-binding sequences upon LPS & CSF1 stimuli in mouse oocytes

Project description:We found that oocytes could arrange IgG production against adverse enviromental stimuli. We want to use chip-seq (cut-and-tag kit) to identify how different stimuli (LPS, CSF1) impact the binding of H3K27ac & H3K4me3 to transcription-regulation sequences of IgG gene

2022-10-30 | GSE191278 | GEO

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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.

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

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

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Computational inference of H3K4me3 and H3K27ac domain length.

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H3K4me3 and H3K27ac ChIp-seq

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