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Sca1+ macrophages activate hematopoietic stem/progenitor cells upon bone marrow stress. [RNA-Seq]

ABSTRACT: Although hematopoietic stem and progenitor cells (HSPCs) become activated in the cell-cycle status after chemotherapy to supply hematopoietic loss, the detailed mechanisms of activation remain unknown. Here we show that Sca1+ macrophages play a key role for bone marrow (BM) recovery through granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion. By analyzing gene expression profiles of HSPCs lodged in 5-fluolouracil (5-FU)-treated mice, we found GM-CSF as a key proliferative signal. Sca1+ macrophages in BM after 5-FU treatment expressed high levels of GM-CSF. GM-CSF-knockout mice treated with 5-FU were lethal because of severe BM suppression. Up-regulation of Csf2 in Sca1+ macrophages by 5-FU was suppressed in MyD88-knockout mice, suggesting that TLR signaling via damage-associated molecular patterns caused by cell death is critical for up-regulation of Csf2. In 5-FU treated BM, majority of Sca1+ macrophages and transplanted HSPCs locate perivascular areas. These findings together indicate that Sca1+ macrophages induce HSPCs to proliferate through GM-CSF signaling in the stressed BM environments.

ORGANISM(S): Mus musculus

PROVIDER: GSE120111 | GEO | 2021/01/20

REPOSITORIES: GEO

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Sca1+ macrophages activate hematopoietic stem/progenitor cells upon bone marrow stress. [scRNA-Seq]

Project description:Although hematopoietic stem and progenitor cells (HSPCs) become activated in the cell-cycle status after chemotherapy to supply hematopoietic loss, the detailed mechanisms of activation remain unknown. Here we show that Sca1+ macrophages play a key role for bone marrow (BM) recovery through granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion. By analyzing gene expression profiles of HSPCs lodged in 5-fluolouracil (5-FU)-treated mice, we found GM-CSF as a key proliferative signal. Sca1+ macrophages in BM after 5-FU treatment expressed high levels of GM-CSF. GM-CSF-knockout mice treated with 5-FU were lethal because of severe BM suppression. Up-regulation of Csf2 in Sca1+ macrophages by 5-FU was suppressed in MyD88-knockout mice, suggesting that TLR signaling via damage-associated molecular patterns caused by cell death is critical for up-regulation of Csf2. In 5-FU treated BM, majority of Sca1+ macrophages and transplanted HSPCs locate perivascular areas. These findings together indicate that Sca1+ macrophages induce HSPCs to proliferate through GM-CSF signaling in the stressed BM environments.

2021-01-20 | GSE120112 | GEO

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Proteome-wide diet-independent adipose tissue alterations link dendritic cells to 2-aminoadipoate associated insulin sensitivity.

Project description:Adipose tissue dysfunction in obese humans is associated with disrupted metabolic homeostasis, insulin resistance, and type 2 diabetes mellitus (T2DM). In a mouse model that has preserved insulin sensitivity despite increased adiposity, we used unbiased three-dimensional integration of proteome profiles, metabolic profiles, and gene regulatory networks to understand adipose tissue proteome-wide changes and their metabolic implications. Multiple-dimensional liquid chromatography tandem mass spectrometry and extended multiplexing TMT labeling (24 biological samples) was used to analyze proteomes of epididymal adipose tissues isolated from wildtype (Csf2+/+) and GM-CSF driven dendritic cell deficient (Csf2-/-) mice that were fed low fat, high fat, or high fat plus cholesterol diets for 8 weeks. The peripheral metabolic health (as measured by body weight, adiposity, plasma fasting glucose, insulin, triglycerides, phospholipids, total cholesterol levels, and glucose and insulin tolerance tests) deteriorated with diet for both genotypes, while mice lacking Csf2 were protected from insulin resistance. Regardless of diet, 30, mostly mitochondrial metabolism proteins participating in amino acid and branched chain amino acid pathways were altered, between Csf2-/- and Csf2+/+ mice. Tissue DHTKD1 levels were >4-fold upregulated and plasma 2-aminoadipoate (2-AA) levels were >2 fold reduced in Csf2-/- mice. GM-CSF driven dendritic cells play a detrimental role in insulin sensitivity via lysine metabolism involving Dhtkd1/2-AA axis.

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2010-02-21 | E-GEOD-14698 | biostudies-arrayexpress

Microarray Experiments for mice lacking or with the Stat5a and 5b genes in blood cells that were treated w/o CMP

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Gene therapy of Csf2ra-/- deficiency in long-term cultured fetal monocyte precursors restores bona fide alveolar macrophage development and function in mice

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2022-01-15 | GSE193537 | GEO

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Microarray analysis of WT bone marrow myeloid progenitors, BM cultured with GM-CSF and M-CSF, and monocytes treated with GM-CSF

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