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PPARγ is essential for the development of erythroblastic island macrophages and red pulp macrophages

ABSTRACT: PPARγ is essential for the development of erythroblastic island macrophages and red pulp macrophages

PROVIDER: PRJNA699241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13619365.fastq.gz	Fastqsanger.gz
	SRR13619366.fastq.gz	Fastqsanger.gz
	SRR13619367.fastq.gz	Fastqsanger.gz
	SRR13619368.fastq.gz	Fastqsanger.gz
	SRR13619369.fastq.gz	Fastqsanger.gz

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Similar Datasets

PPARγ is essential for the development of erythroblastic island macrophages and red pulp macrophages

Project description:Macrophages in the bone marrow erythroblastic island (EIM) and splenic red pulp (RPM) are required for terminal erythropoiesis and removal of aged erythrocytes, respectively. This manuscript shows that EIM and RPM development require both PPARg and Spi-C.

2021-02-04 | GSE166085 | GEO

PPARγ is essential for the development of bone marrow erythroblastic island macrophages and splenic red pulp macrophages.

Project description:Tissue-resident macrophages play a crucial role in maintaining homeostasis. Macrophage progenitors migrate to tissues perinatally, where environmental cues shape their identity and unique functions. Here, we show that the absence of PPARγ affects neonatal development and VCAM-1 expression of splenic iron-recycling red pulp macrophages (RPMs) and bone marrow erythroblastic island macrophages (EIMs). Transcriptome analysis of the few remaining Pparg-deficient RPM-like and EIM-like cells suggests that PPARγ is required for RPM and EIM identity, cell cycling, migration, and localization, but not function in mature RPMs. Notably, Spi-C, another transcription factor implicated in RPM development, was not essential for neonatal expansion of RPMs, even though the transcriptome of Spic-deficient RPMs was strongly affected and indicated a loss of identity. Similarities shared by Pparg- and Spic-deficient RPM-like cells allowed us to identify pathways that rely on both factors. PPARγ and Spi-C collaborate in inducing transcriptional changes, including VCAM-1 and integrin αD expression, which could be required for progenitor retention in the tissue, allowing access to niche-related signals that finalize differentiation.

| S-EPMC8006858 | biostudies-literature

Tissue printing: splenic red pulp macrophages of once-malaria infected mice are transcriptionally identical to prenatally seeded red pulp macrophages from uninfected mice.

Project description:Acute malaria infection with P. chabaudi obliterates embryonically seeded tissue-resident red pulp macrophages in the spleen of C57Bl/6J mice - regardless of whether the infection is mild (mosquito transmitted P. chabaudi AS - no hyperparasitaemia, no measurable clinical manifestations of disease other than low-grade anaemia) or severe (mosquito transmitted P. chabaudi AJ - acute hyperparasitaemia, severe anaemia, hypothermia and prostration). Red pulp macrophages return 100 days later, once mice cleared parasitaemia. We then flow sorted 10,000 red pulp macrophages (lineage-, autofluorescent, F4/80+, B220-, CD11bint, CD11cint) directly into Trizol, extracted total RNA and analysed their transciptome using the affymetrix mouse exon 1.0 ST array. Red pulp macrophages from mice once infected with mild AS or severe AJ P. chabaudi parasites were compared to uninfected age-matched mice. We uncover that red pulp macrophages isolated from the spleens of once-malaria infected mice are transcriptionally identical to prenatally seeded red pulp macrophages from uninfected mice. The spleen tissue niche thus imprints an identical functional profile onto these cells - regardless of their origin.

2020-11-26 | GSE149894 | GEO

Transcript profiling in splenic red pulp macrophages from SIRPa-KO mice and WT mice

Project description:To compare the splenic macrophages between SIRPα-knockout mice and WT mice, we performed a complete transcript profiling of the splenic red pulp macrophages from SIRPα-KO mice compared to WT mice using mRNA microarray as a discovery platform. SIRPα-KO mice and WT mice were kept under the same condition. Macrophages were isolated from spleen red pulp of SIRPα-KO mice and WT mice. RNA was then isolated from the same number of freshly isolated macrophages.

2016-11-22 | GSE78191 | GEO

Transcriptome analysis of erythroblastic island macrophages

Project description:Transcriptome analysis of erythroblastic island macrophages

| PRJNA525977 | ENA

Transcriptome analysis of erythroblastic island macrophages

Project description:The erythroblastic island (EBI), composed of a central macrophage and surrounding erythroid cells, was the first hematopoietic niche discovered. The identity of EBI macrophages has thus far remained elusive. Gene expression profiles of BM F4/80+Epor-eGFP+ macrophages suggest a specialized function in supporting erythropoiesis.

2019-05-31 | GSE127980 | GEO

The role of IL-33 on red pulp macrophage (RPM) development

Project description:This study investigated the effects of IL1RL1 deficiency on the devlopment of red pulp macrophages (RPM)

2020-03-11 | GSE146782 | GEO

Expression data from mouse spleen pre-Red Pulp Macrophages (PreRPM)

Project description:Expression data from mouse spleen pre-Red Pulp Macrophages (PreRPM)

| PRJNA632615 | ENA

Investigation of Bach2 function by heme-iron homeostasis in red-pulp macrophage.

Project description:Macrophages are central in regulating iron homeostasis. Transcription repressor Bach2 regulates by heme. Here we investigated the relationship between heme-regulated Bach2 and macrophage in spleen. We found that gene expression were not many change between WT and Bach2 knock out mice in red-pulp macrophage.Our results suggest that the function of the red-pulp macrophage is not dependent on according to expression of Bach2.

2019-03-31 | GSE79806 | GEO

Differential gene expression of TLR7 overexpressing inflammatory hemophagocytes, Ly6Chi Monocytes, and Red Pulp Macrophages

Project description:We have defined a novel population of monocyte-derived hemophagocytes (inflammatory hemophagocytes (iHPC)) found in situations of inflammation, such as TLR7.1 mice that overexpress TLR7. These iHPC are similar yet distinct from red pulp macrophages (RPM) and differentiate in response to chronic TLR7 signals. In vivo, iHPC phagocytose red blood cells and platelets causing anemia and thrombocytopenia. We performed this study to further understand iHPC and their relationship to RPM and monocytes and determine what gene signatures make them unique.

2019-01-15 | GSE117711 | GEO

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