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Imbalance of Ly6Chi and Ly6Clo monocytes/macrophages worsens hyperoxia-induced lung injury and is rescued by IFN-gamma

ABSTRACT: Imbalance of Ly6Chi and Ly6Clo monocytes/macrophages worsens hyperoxia-induced lung injury and is rescued by IFN-gamma

PROVIDER: PRJNA524824 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8646110.fastq.gz	Fastqsanger.gz
	SRR8646120.fastq.gz	Fastqsanger.gz
	SRR8646130.fastq.gz	Fastqsanger.gz
	SRR8646140.fastq.gz	Fastqsanger.gz
	SRR8646150.fastq.gz	Fastqsanger.gz

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Imbalance of Ly6Chi and Ly6Clo monocytes/macrophages worsens hyperoxia-induced lung injury and is rescued by IFN-gamma

Project description:This study is to examine the transcriptome of mononuclear cell populations in the neonatal lung. We investigated how acute hyperoxia-induced lung injury changes gene expression within these mononuclear populations: dendritic cells, interstitial monocytes/macrophages, and alveolar macrophages.

2022-02-28 | GSE127463 | GEO

Transcription factor C/EBP⍺ is required for the development of Ly6Chi monocytes but not Ly6Clo monocytes

Project description:Monocytes comprise two major subsets, Ly6Chi classical monocytes and Ly6Clo non-classical monocytes. Notch2 signaling in Ly6Chi monocytes triggers transition to Ly6Clo monocytes, which require Nr4a1, Bcl6, Irf2 and Cebpb. By comparison, less is known about transcriptional requirements for Ly6Chi monocytes. We find transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) is highly expressed in Ly6Chi monocytes, but down-regulated in Ly6Clo monocytes. A few previous studies described the requirement of C/EBPα in the development of neutrophils and eosinophils. However, role of C/EBPα for in vivo monocyte development has not been understood. We deleted the Cebpa +37 kb enhancer in mice, eliminating hematopoietic expression of C/EBPα, reproducing the expected neutrophil defect. Surprisingly, we also discovered a severe and selective loss of Ly6Chi monocytes, while preserving Ly6Clo monocytes. We find that BM progenitors from Cebpa +37–/– mice rapidly progress through the cMoP stage to develop directly into Ly6Clo monocytes even in the absence of Notch2 signaling. These results identify a previously unrecognized role for C/EBPα in maintaining Ly6Chi monocyte identity.

2024-03-18 | GSE254202 | GEO

RNA-sequencing analysis of Ly6Chi macrophage and Ly6Clo macrophage harvested from infarcted heart

Project description:C57BL/6 J mice were subjected to ligation of the left anterior descending coronary artery. Ly6Chi macrophages and Ly6Clo macrophages were collected from infarcted hearts at 3 days after MI.

2020-09-27 | GSE115151 | GEO

RNA-seq for blood Ly6Chi and Ly6Clo monocyte in WT and RBP-Jfl/fl Lyz2-Cre mice

Project description:To evaluate the consequences of RBP-J loss of function in blood monocyte subsets, we sequenced RNA of blood Ly6Chi monocyte and Ly6Clo monocyte from WT and RBP-Jfl/fl Lyz2-Cre mice.

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Bcl6, Irf2 and Notch2 promote nonclassical monocyte development [RNA-seq]

Project description:Ly6Clo monocytes are a myeloid subset that specializes in the surveillance of vascular endothelium. Ly6Clo monocytes have been shown to derive from Ly6Chi monocytes. Notch2 signaling has been implicated as a trigger for Ly6Clo monocyte development, but the basis for this effect is unclear. Here, we examined the impact of Notch2 signaling of myeloid progenitors on the development of Ly6Clo monocytes in vitro. Notch2 signaling induced by delta-like ligand 1 (DLL1) efficiently induced the transition of Ly6Chi TremL4– monocytes into Ly6Clo TremL4+ monocytes. We further discovered two additional transcriptional requirements for development of Ly6Clo monocytes. Deletion of Bcl6 from myeloid progenitors abrogated development of Ly6Clo monocyte development. IRF2 was also required for Ly6Clo monocyte development in a cell-intrinsic manner. DLL1-induced in vitro transition into Ly6Clo TremL4+ monocytes required IRF2 but unexpectedly could occur in the absence of Nur77 or Bcl6. These results imply a transcriptional hierarchy for these factors in controlling Ly6Clo monocyte development.

2023-07-28 | GSE218502 | GEO

Bcl6, Irf2 and Notch2 promote nonclassical monocyte development [RNA-Seq]

Project description:Ly6Clo monocytes are a myeloid subset that specializes in the surveillance of vascular endothelium. Ly6Clo monocytes have been shown to derive from Ly6Chi monocytes. NOTCH2 signaling has been implicated as a trigger for Ly6Clo monocyte development, but the basis for this effect is unclear. Here, we examined the impact of NOTCH2 signaling of myeloid progenitors on the development of Ly6Clo monocytes in vitro. NOTCH2 signaling induced by delta-like ligand 1 (DLL1) efficiently induced the transition of Ly6Chi TREML4– monocytes into Ly6Clo TREML4+ monocytes. We further discovered two additional transcriptional requirements for development of Ly6Clo monocytes. Deletion of BCL6 from myeloid progenitors abrogated development of Ly6Clo monocytes. IRF2 was also required for Ly6Clo monocyte development in a cell-intrinsic manner. DLL1-induced in vitro transition into Ly6Clo TREML4+ monocytes required IRF2 but unexpectedly could occur in the absence of NUR77 or BCL6. These results imply a transcriptional hierarchy for these factors in controlling Ly6Clo monocyte development.

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Microarray expression data from bone marrow monocytes and myeloid progenitors

2023-07-28 | GSE218503 | GEO

RNA-sequencing analysis of Ly6Chi macrophage and Ly6Clo macrophage harvested from infarcted heart

Project description:RNA-sequencing analysis of Ly6Chi macrophage and Ly6Clo macrophage harvested from infarcted heart

| PRJNA473977 | ENA

Genome-wide analysis of gene expression of Th1 and Tfh LCMV-specific Smarta CD4 T cell populations

Project description:In this study, we sought to distinguish phenotypically and functionally distinct virus-specific effector CD4 T cell subsets that form during acute lymphocytic choriomeningitis virus (LCMV) infection and to examine their ability to develop into memory T cells. To further characterize the effector subsets and identify genetic pathways and transcription factors involved in their differentiation, we performed genome-wide gene expression profiling of the three day 8 effector cell populations: (1) PSGL1hi Ly6Chi, (2) PSGL1hi Ly6Clo and (3) PSGL1lo Ly6Clo Smarta CD4 T cells along with (4) day 60 memory PSGL1hi and (5) naïve Smarta CD4 T cells using Illumina BeadChips. Results of this microarray confirmed the validity of our phenotyping by flow cytometry in many ways and showed distinct gene signatures for the three effector subsets. DNA microarray analysis was performed on two or three independent samples of five different Smarta CD4 T cell populations: (1) naïSGL1lo, (3) day 8 PSGL1hi Ly6Clo, (4) day 8 PSGL1hi Ly6Clo and (5) day 60 PSGL1hi memory cells.

2011-10-04 | E-GEOD-32596 | biostudies-arrayexpress

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