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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE114291 | GEO | 2019/02/01

REPOSITORIES: GEO

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Single-cell RNA seq reveals the transcriptional landscape and heterogeneity of macrophages in murine gut tissues

Project description:CD11b+ cell populations, especially macrophages are highly heterogeneous tissue resident immune cells in both mice and human. Exact subsets and their phenotype remain unknown. We here analyzed gut CD11b+ cell populations using scRNA-seq in normal, inflamed and Nlrc4 deficient mice. There existed twelve CD11b+ cell populations and subsets in SPF mice. These CD11b+ subsets were changeable dependent on inflammation and gut environment. We found consistent high expression of Ly6C, Cd62L, previously undescribed Trem1 and Ccr7 in Ly6Chigh macrophages and Cd206 and Cx3cr1 in Ly6Clow/neg cell population in different mice. However, signature genes showed that resident macrophages but not inflammatory macrophages were highly conserved in normal and inflamed mice. Gut microbiota play a role in accumulation and differentiation of gut macrophages. Both Ly6Chigh and Ly6Clow macrophages in intestine and colon tissues are similar. These uncover the transcriptional landscape and phenotypic heterogeneity of CD11b+ cells, especially macrophages in gut tissues.

2019-10-16 | GSE138902 | GEO

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

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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.

2019-06-01 | GSE77159 | GEO

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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Single Cell Atlas of Injured Sciatic Nerve Tissue

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2021-11-03 | GSE161467 | GEO

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

Project description:Muscle regeneration is the result of the concerted action of multiple cell types driven by the temporarily controlled phenotype switches of infiltrating monocyte-derived macrophages. Proinflammatory macrophages transition into a phenotype that drives tissue repair through the production of effectors such as growth factors. This orchestrated sequence of regenerative inflammatory events, which we termed Regeneration-Promoting Program (RPP), is essential for proper repair. However, it is not well understood how specialized repair-macrophage identity develops in the RPP at the transcriptional level and how induced macrophage-derived factors coordinate tissue repair. Gene expression kinetics-based clustering of blood circulating Ly6Chigh, infiltrating inflammatory Ly6Chigh, and reparative Ly6Clow macrophages, isolated from injured muscle, identified the TGF-beta superfamily member, GDF-15, as a component of the RPP. Myeloid GDF-15 is required for proper muscle regeneration following acute sterile injury, as revealed by gain- and loss-of-function studies. Mechanistically, GDF-15 acts both on proliferating myoblasts and muscle-infiltrating myeloid cells. Epigenomic analyses of upstream regulators of Gdf15 expression identified that it is under the control of nuclear receptors RXR/PPARg. Finally, immune single-cell RNA-seq profiling revealed that Gdf15 is coexpressed with other known muscle regeneration-associated growth factors, and their expression is limited to a unique subpopulation of repair-type macrophages (Growth Factor-Expressing Macrophages, GFEM).

2021-10-27 | GSE164722 | GEO

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

Project description:Muscle regeneration is the result of the concerted action of multiple cell types driven by the temporarily controlled phenotype switches of infiltrating monocyte-derived macrophages. Proinflammatory macrophages transition into a phenotype that drives tissue repair through the production of effectors such as growth factors. This orchestrated sequence of regenerative inflammatory events, which we termed Regeneration-Promoting Program (RPP), is essential for proper repair. However, it is not well understood how specialized repair-macrophage identity develops in the RPP at the transcriptional level and how induced macrophage-derived factors coordinate tissue repair. Gene expression kinetics-based clustering of blood circulating Ly6Chigh, infiltrating inflammatory Ly6Chigh, and reparative Ly6Clow macrophages, isolated from injured muscle, identified the TGF-beta superfamily member, GDF-15, as a component of the RPP. Myeloid GDF-15 is required for proper muscle regeneration following acute sterile injury, as revealed by gain- and loss-of-function studies. Mechanistically, GDF-15 acts both on proliferating myoblasts and muscle-infiltrating myeloid cells. Epigenomic analyses of upstream regulators of Gdf15 expression identified that it is under the control of nuclear receptors RXR/PPARg. Finally, immune single-cell RNA-seq profiling revealed that Gdf15 is coexpressed with other known muscle regeneration-associated growth factors, and their expression is limited to a unique subpopulation of repair-type macrophages (Growth Factor-Expressing Macrophages, GFEM).

2021-11-16 | GSE182455 | GEO

Gene expression profile at single cell level of leukocytes from transplanted syngeneic left lung grafts following treatment with Resolvin D1.

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2023-07-15 | GSE237110 | GEO

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