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The response to PAM3CSK4 (PAM3) of bone marrow derived macrophages treated with 25-hydroxycholesterol (ChIP-Seq).

ABSTRACT: The response to PAM3CSK4 (PAM3) of bone marrow derived macrophages treated with 25-hydroxycholesterol (ChIP-Seq).

PROVIDER: PRJNA828531 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18837134_1.fastq.gz	Fastqsanger.gz
	SRR18837134_2.fastq.gz	Fastqsanger.gz
	SRR18837135_1.fastq.gz	Fastqsanger.gz
	SRR18837135_2.fastq.gz	Fastqsanger.gz
	SRR18837136_1.fastq.gz	Fastqsanger.gz

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The response to PAM3CSK4 (PAM3) of bone marrow derived macrophages treated with 25-hydroxycholesterol (RNA-Seq).

Project description:Bone marrow derived macrophages from C57BL/6 or Ch25h-/- mice (female) were treated with 25-hydroxycholesterol and then stimulated with PAM3CSK4.

2024-04-03 | GSE201129 | GEO

The response to PAM3CSK4 (PAM3) of bone marrow derived macrophages treated with 25-hydroxycholesterol (ChIP-Seq).

Project description:Bone marrow derived macrophages from C57BL/6 or Ch25h-/- mice (female) were left untreated or treated with 25-hydroxycholesterol for 18 hours and then were left unstimulated or stimulated with PAM3CSK4 for 18 hours. Chromatin was isolated and immunoprecipiation performed for acetyl-H4.

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The response to PAM3CSK4 (PAM3) of bone marrow derived macrophages treated with 25-hydroxycholesterol (RNA-Seq).

Project description:The response to PAM3CSK4 (PAM3) of bone marrow derived macrophages treated with 25-hydroxycholesterol (RNA-Seq).

| PRJNA828533 | ENA

The response to lipopolysaccharide (LPS) of bone marrow derived macrophages treated with oxysterol binding protein (OSBP) inhibitors

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Project description:25-hydroxycholesterol has been demonstrated to regulate SREBP processing, yet Ch25h-deficient mice have no cholesterol abnormalities. Using RNA-seq, we find that LPS-stimulated, Ch25h-deficient BMDMs have dysregulated SREBP target genes, demonstrating that 25-hydroxycholesterol is an induced repressor of SREBP during inflammatory settings. mRNA profiles from day 7 M-CSF bone marrow-derived macrophages (wild type, Ch25h-knockout, LXR-double knockout, were generated by deep sequencing on an Illumina HiSeq 2500. Sequence reads passing a quality filter were aligned to the mouse genome (mm10) using STAR.

2014-08-08 | E-GEOD-58993 | biostudies-arrayexpress

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Lymphatic-derived 25-hydroxycholesterol promotes immunity in melanoma by inhibiting PPAR-γ in tumor associated macrophages and monocytes

Project description:In melanoma, lymphangiogenesis correlates with metastasis and poor prognosis and promotes immunosuppression. However, it also potentiates immunotherapy by supporting trafficking of immune cells. Lymphatic endothelial cells (LECs) are highly plastic cells that shape their phenotype according to distinct microenvironments, which likely define their functional properties, such as immunomodulation. Here, we show in a lymphangiogenic murine melanoma model that LECs upregulate the enzyme Ch25h, which catalyzes the formation of 25-hydroxycholesterol (25-HC) from cholesterol and plays important roles in regulating lipid metabolism, gene expression, and immune activation. LECs represent the main source of extracellular 25-HC in tumors, leading to the inhibition of PPAR- in intra-tumoral macrophages and monocytes. This prevents their immunosuppressive phenotype and instead promotes their conversion into proinflammatory myeloid cells that support effector T cell functions. We identify here in mechanistic detail a novel LEC function that supports anti-tumor immunity, which can be therapeutically exploited in combination with immunotherapy.

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Lymphatic-derived 25-hydroxycholesterol promotes immunity in melanoma by inhibiting PPAR-γ in tumor associated macrophages and monocytes

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Lymphatic-derived 25-hydroxycholesterol promotes immunity in melanoma by inhibiting PPAR-γ in tumor associated macrophages and monocytes

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