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Single cell transcriptomic analysis of hematopoetic stem/progenitor cells (HSPCs) from bone marrow and spleen during hemolytic anemia

ABSTRACT: HSPCs possess multipotent differentiation potential and are responsive to extrinsic stress. In this study, we employed single-cell RNA sequencing (scRNA-seq) to investigate the response of HSPCs to acute blood loss.

ORGANISM(S): Mus musculus

PROVIDER: GSE233845 | GEO | 2023/12/04

REPOSITORIES: GEO

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Single cell transcriptomic analysis of hematopoetic stem/progenitor cells (HSPCs) from bone marrow and spleen during hemolytic anemia

Project description:Single cell transcriptomic analysis of hematopoetic stem/progenitor cells (HSPCs) from bone marrow and spleen during hemolytic anemia

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Transcriptome analysis of HLA-DR(+) HSPCs and HLA-DR(-) HSPCs in aplastic anemia patients

Project description:HLA-DR-lacking HSPCs [HLA-DR(-) HSPCs] were detected in aplastic anemia (AA) patients with HLA-DR15. HLA-DR(-) HSPCs may evade the attack by CD4+ T-cells recognizing the autoantigen presented by HLA-DR15. The goal of this study is to clarify the immune escape mechanisms from antigen-specific T-cells by comparing the trranscriptome profile of HLA-DR(+) HSPCs and HLA-DR(-) HSPCs.

2022-05-31 | GSE183768 | GEO

Investigation of mRNA expression pattern by RAD21 knockdown in hematopoetic stem cells

Project description:Elevated inflammation represents a hallmark of hematopoietic aging and leukemia development but mechanistically its impact on hematopoietic stem and progenitor cell (HSPC) maintenance remains incompletely understood. Here we identify Rad21/cohesin as a major component mediating inflammation-induced NF-kB signaling, which in turn limits self-renewal of HSPCs by induction of differentiation. Disruption of Rad21/cohesin diminishes inflammation-induced loss of self-renewal and induction of differentiation, but these effects are abrogated in NF-kB knockout (p50-/-) HSPCs. During aging, HSPCs exhibit an increased responsiveness to activate NF-kB signaling in response to inflammatory stimuli also resulting in activation of genes encoding for secreted cytokines. These cell intrinsic and extrinsic responses cooperatively enhance differentiation and loss of self-renewal of HSPCs resulting in increased selection of Rad21/cohesin deficient HSPCs exhibiting elevated self-renewal and myeloid skewed differentiation. Together, these results identify cohesin-mediated NF-kB signaling as a major axis connecting cell extrinsic increases in inflammation with the evolution of hallmark features HSC aging characterized by increases in self renewal and myeloid skewed differentiation aggravated by the concomitant selection of cohesin deficient HSPCs.

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Transcriptome analysis of HLA-DR(+) HSPCs and HLA-DR(-) HSPCs in aplastic anemia patients

Project description:Transcriptome analysis of HLA-DR(+) HSPCs and HLA-DR(-) HSPCs in aplastic anemia patients

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Time series single-cell RNA sequencing of murine hematopoetic stem and progenitors (HSPCs) following in vivo IFNα treatment

Project description:The molecular and cellular dynamics of hematopoietic stem and progenitor cells (HSPCs) during the course of inflammation remain poorly studied. It has been challenging to characterize inflammation in HSPCs due to changes in cell type-specific surface markers. To address this challenge, we performed single-cell RNA sequencing of HSPCs at multiple time points (3, 24, and 72 hours) after treatment with the pro-inflammatory cytokine IFNα and developed a computational pipeline suitable for processing and analyzing single-cell time series dataset. Using a semi-supervised response-pseudotime inference approach, we discover a variety of different gene responses of the HSPCs to the treatment. Interestingly, we were able to associate the myeloid abundance changes with downregulated myeloid differentiation programs in HSCs and progenitors following IFNα treatment. Using single-cell time series we have been able to unbiasedly study the heterogeneous and dynamic impact of IFNα on the HSPCs

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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.

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Project description:Haematopoietic stem and progenitor cells (HSPCs) in the foetus and adult possess distinct molecular landscapes that regulate cell fate and change their susceptibility to initiation and progression of haematopoietic malignancies. The proteomic programs that govern these differences remain elusive. In this study, we have utilized a mass spectrometry-based quantitative proteomics approach to comprehensively describe and compare the proteome of foetal and adult HSPCs. We found that the proteome of foetal HSPCs is relatively simple, characterized by proteins involved in cell cycle and cell proliferation, while their adult counterparts are defined by a larger set of proteins that are involved in more diverse cellular processes. These adult characteristics include an arsenal of proteins important for viral and bacterial defence, as well as protection against ROS-induced protein oxidation. Our further analyses of Type I interferon signalling shows that foetal HSPCs are sensitive to Interferon a (IFNa), which impairs their production of mature lymphoid cells, whereas stimulation with IFNa to the pregnant mother enhances the production of early progenitors from foetal HSCs. Our results provide new and important insights into the molecular landscape of foetal and adult haematopoiesis that advance our understanding of normal and malignant haematopoiesis during foetal and adult life.

2017-12-12 | PXD006876 | Pride

Transcriptional landscape, long non-coding RNAs and post-transcriptional regulation in hematopoietic stem/progenitor cell differentiation

Project description:Hematopoietic stem cells (HSC) possess life-long self-renewal activity and generate a series of multipotent progenitors that differentiate into lineage-committed progenitors and subsequently mature cells. Recently, functionally distinct stem and progenitor cell types have been identified, however, a systems-wide understanding of the underlying gene regulation is lacking. Here, we present the global transcriptome of ex vivo isolated mouse multipotent hematopoietic stem/progenitor cells (HSPCs, LinnegSca-1+c-Kit+) and myeloid committed precursors (LinnegSca-1-c-Kit+) as revealed by next-generation sequencing (RNA-seq).

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Murine fetal bone marrow does not support functional hematopoietic stem and progenitor cells until birth

Project description:Fetal hematopoietic stem and progenitor cells (HSPCs) migrate from fetal liver (FL) to bone marrow (BM) around birth. While adult BM HSPCs and their extrinsic regulation is well studied, little is known about the composition, function, and extrinsic regulation of the first HSPCs to enter the BM. Here, we show that HSPCs colonize multiple fetal bones by E15.5, shift from an MPP2 to an MPP3/4-dominant phenotype by birth, and display little function until E18.5, relative to their FL counterparts. We establish a transcriptional atlas of single perinatal HSPCs, and their putative BM niches, from E15.5 through P0 and show that early fetal BM (FBM) lacks HSPCs with intrinsic stem cell programs and niche cells supportive of HSPCs. In contrast, stem cell programs are preserved in neonatal BM HSPCs, which engage with a niche expressing HSC supportive factors distinct from those seen in adult BM (i.e., IGF).

2021-06-26 | GSE178951 | GEO

Autoimmune hemolytic anemia.

Project description:The diagnosis of autoimmune hemolytic anemia (AIHA) can be made with a stepwise approach that aims to identify laboratory and clinical evidence of hemolysis and then determine the immune nature of hemolysis with the direct anti-globulin test. Once alternative causes for these findings have been excluded, AIHA is established, and the clinician must search for secondary causes, as well as identify the type of AIHA. Rituximab is now the preferred second-line treatment for primary warm AIHA and first-line treatment for primary cold agglutinin disease (CAD), either as monotherapy or combined with bendamustine. Complement inhibitors have shown utility in stabilizing AIHA patients with acute severe hemolysis. Future prospects are discussed and include the C1s inhibitor BIVV009 (sutimlimab) that is now entering phase 3 studies for CAD.

| S-EPMC6246027 | biostudies-literature

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