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Mus musculus

ABSTRACT: RNA-seq of IL-4 complex treated tissue resident macrophages vs. monocytic macrophages from LysM Cre+ (WT litermate control) and LysM Cre+ RICTOR KO (myeloid specifically RICTOR deleted) mice

PROVIDER: PRJNA374962 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5261130_1.fastq.gz	Fastqsanger.gz
	SRR5261130_2.fastq.gz	Fastqsanger.gz
	SRR5261131_1.fastq.gz	Fastqsanger.gz
	SRR5261131_2.fastq.gz	Fastqsanger.gz
	SRR5261132_1.fastq.gz	Fastqsanger.gz

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RNA-seq of IL-4 complex treated tissue resident macrophages vs. monocytic macrophages from LysM Cre+ (WT litermate control) and LysM Cre+ RICTOR KO (myeloid specifically RICTOR deleted) mice

Project description:RNA-seq was performed on sorted peritoneal tissue resident macrophages (CD11b+F4/80hiTIM4+) and monocytic macrophages (CD11b+F4/80loTIM4-) from IL-4c (recombinant IL-4 (5µg) and anti-IL-4 ab (12.5µg) IP injection on days 0 and 2 and sorted on day 4) treated 6-8wks old LySM Cre+ and LysM Cre+ RICTOR KO (C57BL/6 background) for expression profiling

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Inactivation of mTORC2 in macrophages is a signature of colorectal cancer that promotes tumorigenesis.

Project description:Gene expression analysis of sorted colon macrophages of Rictor fl/fl LysM+/+ and Rictor fl/fl LysM+/cre mice Dysregulations of immune and metabolic processes can lead to chronic inflammation, which is one of the driving forces for the development of cancer. Macrophages are regulators of these processes and therefore have a fundamental role for the initiation of cancer. Here we find that deletion of Rictor in myeloid cells increases tumor number and size in the colitis-associated colorectal cancer model and leads to a stronger inflammatory response in the underlying acute DSS-colitis model. OPN is shown to be upregulated in the serum of myeloid-specific Rictor-KO mice during the DSS-colitis and the more severe phenotype, characterized by decreased survival, increased weight loss, shorter colons and enhanced infiltration of immune cells into the colon, can be reverted by the neutralization of OPN in these mice. Microarray analysis reveals a change in inflammatory and metabolic gene signatures of Rictor-KO colon macrophages that is also seen in the Rictor-KO BMDM in vitro. Therefore, our data show that myeloid Rictor controls macrophage polarization and the cellular energy metabolism, thereby suppressing colitis and colitis-associated colorectal cancer.

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Project description:Macrophages were derived from the bone-marrow of 3 x fl/+ Dicer LysCre +/- (wild-type) and 3 x fl/fl Dicer LysCre +/- mice and stimulated with IL-4 (50ng/mL) for 72h. Total RNA was isolated and analyzed by gene array. In this experiment, we derived Dicer deficient bone-marrow macrophages using Dicer fl/+ LysM-Cre by Dicer fl/+ crossed mice to obtain Dicer fl/fl LysM-cre progeny (and Dicer deficient macrophages). Next, we studied the effects of IL-4 stimulation in macrophage with a deficiency in Dicer/microRNAs.

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Project description:We sequenced microRNAs from bone marrow derived macrophages derived from the control (WT) and RBP-J conditional knockout mice (RBP-J KO; Rbpjf/f; LysM Cre).

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Project description:We sequenced microRNAs from bone marrow derived macrophages derived from the control (WT) and RBP-J conditional knockout mice (RBP-J KO; Rbpjf/f; LysM Cre). Examination of differential microRNA expression levels induced by TNF as well as regulated by RBP-J in bone marrow derived macrophages.

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