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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE166085 | GEO | 2021/02/04

REPOSITORIES: GEO

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

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

| PRJNA699241 | ENA

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

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.

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Transcriptome analysis of erythroblastic island macrophages

Project description:Transcriptome analysis of erythroblastic island macrophages

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Burn Injury-Induced G-CSF Secretion Depletes Spi-C+ Erythroblastic Island Macrophages and Impairs Medullary Erythropoiesis.

Project description:The erythroblastic island (EBI) functions as a niche where erythroblastic island macrophages (EBIMφ) are positioned within rings of erythroblasts, providing support and signals that orchestrate efficient erythropoiesis. Herein, we postulated burn injury impacts the EBI, given the nearly universal presence of anemia and inflammation in burn patients, and a divergent myeloid transcriptional signature we observed in murine bone marrow following burn injury, where G-CSF secretion increased neutrophil and monocyte transcripts but reduced EBIMφ transcripts. We utilized flow cytometry to investigate EBIMφ after imaging flow cytometry confirmed the heme induced transcription factor Spi-C as a robust marker of EBIMφ in Spicigfp/igfp mice. Two populations referred to as Spic+ macrophages and Spic+ Gr1 low monocytes possessed cell intrinsic GFP, with Spic+ macrophages distinguished by higher levels of GFP, F4/80, autofluorescence, and negligible CD115 staining compared to Gr1 low monocytes. Further, at least 50% of the Spic+ macrophages stained for CD163 while staining was negligible on Gr1 low monocytes. Since CD163 distinguished the populations and macrophage remnants could convolute flow cytometry analysis, total CD163 protein was quantified in marrow aspirates to corroborate results. Application of Spicigfp/igfp mice in studies revealed a G-CSF dependent reduction of Spic+ macrophages in post burn marrow that coincided with a loss of erythroid cells and that recombinant G-CSF alone was sufficient to reduce Spic+ macrophages in the marrow. These results provide the first evidence that burn injuries impact the EBI niche through G-CSF dependent depletion of EBIMφ and support the use of Spicigfp/igfp mice in investigation of EBIMφ.

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Burn Injury-Induced G-CSF Secretion Depletes Spi-C+ Erythroblastic Island Macrophages and Impairs Medullary Erythropoiesis.

Project description:Burn Injury-Induced G-CSF Secretion Depletes Spi-C+ Erythroblastic Island Macrophages and Impairs Medullary Erythropoiesis.

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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.

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Heme regulates the development of iron-recycling macrophages from monocytes (sorted splenocytes)

Project description:Splenic red pulp macrophages (RPM) degrade senescent erythrocytes and recycle heme-associated iron. The transcription factor Spic is selectively expressed by RPM and is required for their development, but the physiologic stimulus inducing Spic is unknown. Here, we report that Spic also regulated the development of F4/80+VCAM+ bone marrow macrophages (BMM) and that Spic expression in BMM and RPM development was induced by heme, a metabolite of erythrocyte degradation. Pathologic hemolysis induced loss of RPM and BMM due to excess heme but induced Spic in monocytes to generate new RPM and BMM. Spic expression in monocytes was constitutively inhibited by the transcriptional repressor Bach1. Heme induced proteasome-dependent BACH1 degradation and rapid Spic derepression. Further, cysteine-proline dipeptide motifs in BACH1 that mediate heme-dependent degradation were necessary for Spic induction by heme. These findings are the first example of metabolite-driven differentiation of a tissue-resident macrophage subset and provide new insight into iron homeostasis. Global gene expression pattern of Spic+ monocytes, Spic- monocytes, and Spic high red pulp macrophages were compared by sorting these cells from Spic(igfp/+) splenocytes and performing microarray-based gene expression profiling.

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The erythroblastic island.

Project description:Erythroblastic islands are specialized microenvironmental compartments within which definitive mammalian erythroblasts proliferate and differentiate. These islands consist of a central macrophage that extends cytoplasmic protrusions to a ring of surrounding erythroblasts. The interaction of cells within the erythroblastic island is essential for both early and late stages of erythroid maturation. It has been proposed that early in erythroid maturation the macrophages provide nutrients, proliferative and survival signals to the erythroblasts, and phagocytose extruded erythroblast nuclei at the conclusion of erythroid maturation. There is also accumulating evidence for the role of macrophages in promoting enucleation itself. The central macrophages are identified by their unique immunophenotypic signature. Their pronounced adhesive properties, ability for avid endocytosis, lack of respiratory bursts, and consequent release of toxic oxidative species, make them perfectly adapted to function as nurse cells. Both macrophages and erythroblasts display adhesive interactions that maintain island integrity, and elucidating these details is an area of intense interest and investigation. Such interactions enable regulatory feedback within islands via cross talk between cells and also trigger intracellular signaling pathways that regulate gene expression. An additional control mechanism for cellular growth within the erythroblastic islands is through the modulation of apoptosis via feedback loops between mature and immature erythroblasts and between macrophages and immature erythroblasts. The focus of this chapter is to outline the mechanisms by which erythroblastic islands aid erythropoiesis, review the historical data surrounding their discovery, and highlight important unanswered questions.

| S-EPMC3234703 | biostudies-literature

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