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Mus musculus

ABSTRACT: Triggering of NOD2 receptor converts inflammatory Ly6Chigh into Ly6Clow monocytes with patrolling properties.

PROVIDER: PRJNA394681 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5831460_1.fastq.gz	Fastqsanger.gz
	SRR5831460_2.fastq.gz	Fastqsanger.gz
	SRR5831470_1.fastq.gz	Fastqsanger.gz
	SRR5831470_2.fastq.gz	Fastqsanger.gz
	SRR5831461_1.fastq.gz	Fastqsanger.gz

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Triggering of NOD2 receptor converts inflammatory Ly6Chigh into Ly6Clow monocytes with patrolling properties.

Project description:In the present study, we demonstrate that NOD2 receptor triggering by muramyl dipeptide converts blood inflammatory Ly6Chigh monocytes into patrolling Ly6Clow monocytes. Muramyl dipeptide administration to Nr4a1-/- mice, which lack Ly6Clow monocytes, and to Ly6Clow-depleted mice leads to the emergence of blood patrolling monocytes expressing phenotypic profile of typical Ly6Clow monocytes, including high expression of CX3CR1 and LFA1. Furthermore using intravital microscopy in live animal models of inflammatory diseases, we observed that converted Ly6Chigh monocytes are capable of patrolling the endothelium of blood vessels and their presence contributes to reduce the inflammatory response following muramyl dipeptide injection.

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Identification of miR-146a target genes in mouse monocyte subsets

Project description:To gain insight into the mechanisms underlying miR-146a-mediated modulation of Ly6Chigh monocyte function, we compared the expression profiles of Ly6Chigh and Ly6Clow monocytes in miR-146a+/+ (WT) versus miR-146a-/- (KO) conditions.

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Ly6C monocyte subsets transcriptome analysis from wild type and hyperhomocysteinemic mice

Project description:Murine monocytes (MC) are classified into Ly6Chigh and Ly6Clow MC. Ly6Chigh MC is the pro-inflammatory subset and the counterpart of human CD14++CD16+ intermediate MC which contributes to systemic and tissue inflammation in various metabolic disorders, including hyperhomocysteinemia (HHcy). This study aims to explore molecule signaling mediating MC subset differentiation in HHcy and control mice.Mouse white blood cell were prepared from peripheral blood and stained with antibody against CD11b, Ly6G and Ly6C and subjected for flow cytometry cell sorting. CD11b+Ly6G- cells were selected as MC. MC subsets (CD11b+Ly6G-Ly6Chigh, and CD11b+Ly6G-Ly6Clow) were sorted based on Ly6C levels. The quantification of MC was used flow cytometry analysis for Ly6Chigh and Ly6Clow MC in CT and Cbs-/-. Then, 100 ng mRNA were obtained from 100,000 sorted cells of CT and Cbs-/- (HHcy) mice. Around 30 million reads were achived and 16,487 normalized genes per sample by mRNA-Seq analysis.

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Transcriptional analysis on the impact of anti-PD-L1 mAb on murine lung tumor sorted myeloid populations.

Project description:Targeted gene expression on Lewis lung carcinoma (LLC) sorted MHC-IIlow macrophages (M2), Ly6Chigh inflammatory (IM) and Ly6Clow residential (RM) monocytes to investigate the effect of anti-PD-L1 mAb on specific myeloid subsets in the lung tumor microenvironment performed using the nCounter Myeloid Innate Immunity Panel by Nanostring .

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Dynamic lipid mediator changes support infiltrating macrophage subtype transitions during skeletal muscle injury and regeneration

Project description:Time-dependent profiles were recapitulated in sorted neutrophils and Ly6Chigh and Ly6Clow muscle macrophages, with a distinct pro-resolving signature observed in Ly6Clow reparative macrophages. RNA-seq analysis of macrophages stimulated with resolvin D2 (RvD2) showed similarities to transcriptional changes found during the temporal Ly6Chigh to Ly6Clow phenotypic transition. Importantly, RvD2 promoted the temporal progression from Ly6Chigh to Ly6Clow macrophages in vivo.

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Targeted deletion of an Nr4a1 associated enhancer ablates Ly6Clow monocytes while protecting pleiotropic gene function in macrophages [RNA-seq]

Project description:Mononuclear phagocytes are a diverse cell family that occupy all tissues and assume numerous functions to support tissue and systemic homeostasis. Our ability to investigate the roles of individual subsets is limited by an absence of approaches to ablate gene function within specific sub-populations. Using Nr4a1-dependent Ly6Clow monocytes as a representative cell type we show that enhancer deletion addresses these limitations. Combining ChIP-Seq and molecular approaches we identify a single, conserved, sub-domain within the Nr4a1 enhancer that is essential for Ly6Clow monocyte development. Mice lacking this enhancer lack Ly6Clow monocytes but retain Nr4a1 gene expression in macrophages during steady state and in response to LPS. Nr4a1 is a key negative regulator of inflammatory gene expression and decoupling these processes allows Ly6Clow monocytes to be studied without confounding influences. Enhancer targeting possesses greater specificity than cre recombinase-mediated gene deletion, providing a route to generate loss-of-function models in closely related cell types.

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