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Bone marrow HSPCs differentiate into myeloid cells in depression

ABSTRACT: Bone marrow HSPCs differentiate into myeloid cells in depression

PROVIDER: PRJNA1048970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27089330_1.fastq.gz	Fastqsanger.gz
	SRR27089330_2.fastq.gz	Fastqsanger.gz
	SRR27089331_1.fastq.gz	Fastqsanger.gz
	SRR27089331_2.fastq.gz	Fastqsanger.gz
	SRR27089332_1.fastq.gz	Fastqsanger.gz

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Bone marrow HSPCs differentiate into myeloid cells in depression

Project description:It has been known that the numbers of neutrophils and Ly6Chi monocytes are increased in the blood of patients with depression. To better understand how HSPCs sense and adapt disease progression in depression, we used single-cell RNA sequencing (scRNA-seq) to characterize HSPCs in bone marrow from mice models of depression induced by chronic restraint stress (CRS) and chronic unpredictable mild stress (CUMS).We found that bone marrow hematopoiesis was substantially rewired toward myeloid lineages in depression, accompanied by an increase of myeloid score in bone marrow HSPCs, suggesting myeloid biased cell production in bone marrow of depressed mice.

2024-12-01 | GSE249396 | GEO

AVP promotes bone marrow myelopoiesis in depression

Project description:AVP promotes bone marrow myelopoiesis in depression

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Single-cell RNA sequencing of bone marrow HSPCs isolated from patients after myocardial infarction and control patients

Project description:This experiment focused on studying the impact of myocardial infarction on bone marrow HSPCs (LineageNeg, CD38Neg, CD34Pos). Human sternal bone marrow was extracted from the sternum of acute patients who had undergone myocardial infarction (n = 6), as well as from control patients (n = 7), during surgical procedures.

2025-02-05 | E-MTAB-13509 | biostudies-arrayexpress

scRNAseq of bone marrow (BM) T cells and hematopoietic stem and progenitor cells (HSPCs) of acute myeloid leukemia patients post allogeneic stem cell transplantation (alloSCT).

Project description:Gene expression profile at single cell level of bone marrow (BM) T cells and hematopoietic stem and progenitor cells (HSPCs) of acute myeloid leukemia patients post allogeneic stem cell transplantation (alloSCT) of patients in complete remission (CR) and relapse (REL).

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MYC Promotes Bone Marrow Stem Cell Dysfunction in Fanconi Anemia

Project description:We profiled primary HSPCs from Fanconi anemia (FA) patients for single cell transcriptome (scRNA-seq) to identify additional determinants of HSPC impairment leading to the bone marrow failure,. Trajectory analysis revealed that early hematopoietic differentiation potential is preserved in FA HSPCs. As expected, p53 and TGFβ pathway genes were overexpressed in HSPCs from FA patients. The oncogene MYC was also identified as one of the top over-expressed genes in FA HSPCs. Interestingly, we observed co-existence of “High-TP53” expressing HSPCs and HighMYC expressing HSPCs in FA bone marrow. Inhibition of MYC expression by the BET bromodomain inhibitor (+)-JQ1 reduced the clonogenic potential of primary HSPCs from FA patients but rescued the physiological/genotoxic stress in HSPCs from FA mice. The “High-MYC” expressing HSPCs exhibited a significant downregulation of cell adhesion genes, such as CXCR4. Consistently, HSPCs in FA patients showed a defect in adhesion to their bone marrow niche resulting in egression from the bone marrow into peripheral blood. We speculate that MYC overexpression impairs HSPC function and contributes to exhaustion of HSPCs in FA bone marrow.

2020-09-08 | GSE157591 | GEO

AVP promotes bone marrow myelopoiesis in depression

Project description:Sympathetic nerves have been implicated in the regulation of HSC homeostasis, we investigated whether sympathetic nerves regulated myeloid-biased differentiation of HSCs in CUMS mice. Transcriptome profiling (RNA-seq) and differential gene expression analysis of bone marrow cells were performed. In bone marrow cells of CUMS mice, the expression of arginine vasopressin receptor 2, a receptor of the stress-related neuroendocrine factor AVP, was upregulated through neuroactive ligand-receptor interaction pathway.

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Project description:Metabolic cues are crucial for regulating hematopoietic stem and progenitor cells (HSPCs). However, the metabolic profile of human HSPCs remains poorly understood due to the limited number of cells and the scarcity of bone marrow samples. Here, we present the integrated metabolome, lipidome and transcriptome of human adult HSPCs (lineage-, CD34+, CD38-) upon differentiation, aging and acute myeloid leukemia (AML). The combination of low-input targeted metabolomics with our newly optimized low-input untargeted lipidomics workflow allows us to detect up to 219 metabolites and lipids from a starting material of 3,000 and 5,000 HSPCs, respectively. Among other findings, we observe elevated levels of the essential nutrient choline in HSPCs compared to downstream progenitors, which decline upon aging and further decrease in AML. Functionally, we show that choline supplementation fuels lipid production in HSPCs and enhances stemness. Overall, our study provides a comprehensive resource identifying metabolic changes that can be utilized to promote and enhance human stem cell function.

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Project description:Two subsets of dendritic cell (DCs), plasmacytoid (p) and myeloid (m) DCs, have been described in humans and mice. These subsets are known to have divergent roles during an immune response, but their developmental course is unclear. Here we report that virus infection induces bone marrow pDCs to differentiate into mDCs, thereby undergoing profound phenotypic and functional changes including the acquisition of enhanced antigen-presenting capacity and the ability to recognize different microbial structures through Toll-like receptor 4. The conversion of pDCs into mDCs is also induced by the injection of double-stranded RNA and requires type I interferons. Our results establish a precursor-product developmental relationship between these two DC subsets and highlight unexpected plasticity of bone marrow pDCs.

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Project description:The TLR9-/- mice had more myeloid cells and progenitors and fewer B cells in the bone marrow. Activity of Fos and Cebpb, important mediator of myelopoiesis, in the cluster of HSPCs were increased. PU.1 and Fos, critical transcription factors mediating osteoclastogenesis, were upregulated in monocyte progenitors. In addition to myeloid biased hematopoiesis in TLR9-/- mice, there were upregulated levels of inflammatory cytokines in the TLR9-/- bone marrow.

2022-06-01 | GSE166366 | GEO

Expression data from Bone marrow and Fetal liver Lineage-c-Kit+Sca-1+ (LSK) cells

Project description:Loss of polycomb-group gene Ezh2 causes activation of fetal gene signature in adult mouse bone marrow (BM) hematopoietic stem and progenitor cells (HSPCs). Ezh2 directly represses fetal-specific let-7 target genes, including Lin28, thereby cooperates with let-7 microRNAs in silencing fetal gene signature in BM HSPCs. We purified Lineage-Sca-1+c-Kit+ (LSK) HSPCs from E14.5 FL and adult BM and subjected them to microarray analysis.

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