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469 results for “Hematopoiesis”
Fig. 1 in Pecular Features Of Hematopoiesis In The Liver Of Mature And Immature Green Frogs (Pelophylax Esculentus Complex)
Fig. 1. Smear-imprint of the liver of immature green frog: a — pigment cells; b — erythroblasts; c — undifferentiated blast, erythroblast and eosinophilicmyelocyte; d — erythroblast and medullocell neutrophil. Pappenheim staining, ×200.
ETV6 represses Tumor Necrosis Factor During Stress Hematopoiesis to Regulate Mouse Stem Cell Function
<p>At the root of the blood system lies a heterogenous population of hematopoietic stem and progenitor cells (HSPCs), which reside in the bone marrow (BM) and give rise to diverse blood lineages. Maintaining this pool of self-renewing HSPCs is critical to uphold hematopoiesis during period of stress such as bleeding or infection<sup>1</sup>. ETS Variant Transcription Factor 6 (ETV6) is a transcriptional repressor that is highly expressed in HSPCs<sup>2</sup> where it is essential for development and maintenance of the adult hematopoiesis <sup>3</sup>. In 2015, our group<sup>4</sup> and others<sup>5-7</sup> identified germline pathogenic <em>ETV6</em> variants in families with predisposition to B-acute lymphoblastic leukemia (B-ALL) and thrombocytopenia, defining a new genetic syndrome known as Thrombocytopenia 5 (T5). Subsequently, we performed targeted germline <em>ETV6 </em>sequencing of remission blood samples from over 4,000 children with B-ALL and identified germline <em>ETV6</em> variants in ~1% of cases<sup>7</sup>. <em>In vitro</em> studies revealed that ETV6 variant proteins exhibit impaired repressor activity, reduced DNA binding, and aberrant subcellular localization<sup>4,5,7,8</sup>. Overall, these studies indicated that T5-associated germline <em>ETV6</em> variants negatively impact the repressor activity of ETV6. In support of this notion, transcriptional profiling of peripheral blood cells from T5 patients has revealed upregulation of interferon response genes<sup>9</sup>. Nevertheless, little remains known about the mechanisms by which ETV6 regulates the HSPC compartment and how T5-associated <em>ETV6</em> variants contribute to disease.</p> <p> </p> <p>To address these questions, we used CRISPR-Cas9 gene editing to generate a novel mouse model harboring a pathogenic heterozygous germline <em>Etv6 </em>variant, R355X, the murine equivalent to the human T5-associated variant R359X<sup>10</sup>. Through the comprehensive study of this model, we describe a novel role for ETV6 during aging and regenerative hematopoiesis and show that the heterozygous <em>Etv6</em><sup>R355X</sup> variant impairs HSC function <em>in vitro</em> and <em>in vivo</em>. Using genomic approaches to interrogate mouse and human HSCs, we identify new ETV6 targets, including the gene encoding Tumor Necrosis Factor (TNF) and genes involved in TNF signaling. Further, we show increased TNF production and cell cycling in <em>Etv6<sup>R355X/+</sup></em> mouse HSPCs post-BM transplantation. Finally, we demonstrate that genetic ablation of <em>Tnf</em> restores the long-term potential of <em>Etv6<sup>R355X/+</sup></em> cells in serial replating assays <em>in vitro</em>. Together, these findings provide novel insights into the pathways regulated by ETV6 and demonstrate how a pathogenic variant impacts ETV6 function in the context of hematopoietic stress.</p> <p>All bulk RNAseq, Cut&Run, ATACseq, and Hi-C data has been submitted to in the Gene Expression Omnibus (accession number GSE213597) and Sequence Read Archive (BioProject number PRJNA880871). Due to the journal’s limitation on submitted supplementary data as an Excel file, all post-analysis supplemental data files are deposited in Dryad data repository to be made available with this manuscript.</p>
Injectable, Scalable 3D Tissue-Engineered Model of Marrow Hematopoiesis
<p>Raw data associated with the publication "<strong>Injectable, Scalable 3D Tissue-Engineered Model of Marrow Hematopoiesis"</strong></p> <p><a href="https://www.sciencedirect.com/science/article/pii/S0142961219307641"><strong>DOI: 10.1016/j.biomaterials.2019.119665</strong></a></p>
A Study to Investigate the Efficacy, Safety, and Tolerability of DFV890 and MAS825 for Inflammatory Marker Reduction in Adult Participants With Coronary Heart Disease and Clonal Hematopoiesis of Indet
ClinicalTrials.gov study NCT06097663. IPD Sharing: YES. Countries: 3. Publications: 1.
Non-Canonical Hedgehog Signaling Mediates Profibrotic Hematopoiesis-Stroma Crosstalk in Myeloproliferative Neoplasms
<p>We provide results regarding the bioinformatic analysis of scRNA-seq from bone marrow fibrosis mouse models. This includes final processed scRNA-seq data containing QC information, dimensionality reduction, and annotation of cell types. Additional tables including DE genes and markers can be found in the supplementary information of the publication.</p>
Clonal hematopoiesis GWAS summary statistics
<p>Datasets linked to the pre-print titled, "Genome-wide analyses of 200,453 individuals yields new insights into the causes and consequences of clonal hematopoiesis", which is available at <a href="https://doi.org/10.1101/2022.01.06.22268846">https://doi.org/10.1101/2022.01.06.22268846</a></p> <p>To estimate odds ratios from BOLT-LMM betas and standard errors please use the formula provided <a href="https://alkesgroup.broadinstitute.org/BOLT-LMM/BOLT-LMM_manual.html#x1-5500010.2">here</a>. The formula requires the number of controls (= 173,918 for each of the five GWAS) and the numbers of cases (10,203 overall-CH, 5,185 DNMT3A-CH, 2,042 TET2-CH, 4,049 large-CH, and 6,154 small-CH).</p>
Data from: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice
<p>The investigation of the mechanisms behind p53 mutations in acute myeloid leukemia (AML) has been limited by the lack of suitable mouse models, which historically have resulted in lymphoma rather than leukemia. This study introduces two new AML mouse models. One model induces mutant p53 and <em>Mdm2</em> haploinsufficiency in early development, showing the role of Mdm2 in myeloid-biased hematopoiesis and AML predisposition, independent of p53. The second model mimics clonal hematopoiesis by inducing mutant p53 in adult hematopoietic stem cells, demonstrating that the timing of p53 mutation determines AML versus lymphoma development. In this context, age-related changes in hematopoietic stem cells (HSCs), collaborates with mutant p53 to predispose towards myeloid transformation rather than lymphoma development. Our study unveils new insights into the cooperative impact of HSC age, <em>Trp53</em> mutations and <em>Mdm2</em> haploinsufficiency on clonal hematopoiesis and the development of myeloid malignancies.</p>
The evolutionary dynamics and fitness landscape of clonal hematopoiesis
Open the record for dataset details and reuse information.
Data from: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice
Open the record for dataset details and reuse information.
Clonal Hematopoiesis of Indeterminate Potential and Accelerated Atherosclerosis in Systemic Lupus Erythematosus
ClinicalTrials.gov study NCT05146414. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Epigenetics, Vitamin C and Abnormal Hematopoiesis - Pilot Study
ClinicalTrials.gov study NCT02877277. IPD Sharing: NO. Countries: 1. Publications: 1.
Clonal Hematopoiesis is a Risk Factor for Chemotherapy-Related Complications
ClinicalTrials.gov study NCT04053439. IPD Sharing: NO. Countries: 1. Publications: 5.
Aging of Hematopoietic Stem Cells - Molecular Architecture of Marrow Dysplasia and Clinical Contribution of Ineffective Hematopoiesis to Frailty in the Elderly
ClinicalTrials.gov study NCT03907553. IPD Sharing: NO. Countries: 1. Publications: 52.
Correlation Between Clonal Hematopoiesis, Cardio-vascular Events, Inflammation and Atherosclerosis
ClinicalTrials.gov study NCT04581057. IPD Sharing: NO. Countries: 1. Publications: 1.
Study Investigating the Interactions of Bone and Hematopoiesis in the Elderly
ClinicalTrials.gov study NCT02867085. IPD Sharing: NO. Countries: 1. Publications: 1.
Clonal Hematopoiesis of Indeterminate Potential in Venous Thromboembolism
ClinicalTrials.gov study NCT04477564. IPD Sharing: NO. Countries: 1. Publications: 1.
PPG Project 3 - PET/MRI of the Brain-hematopoiesis-atherosclerosis Axis in PTSD Patients
ClinicalTrials.gov study NCT03279393. IPD Sharing: YES. Countries: 1. Publications: 15.
Regenerative Medicine to Restore Hematopoiesis and Immune Function in Immunodeficiencies and Inherited Bone Marrow Failures
ClinicalTrials.gov study NCT04232085. IPD Sharing: NO. Countries: 1. Publications: 1.
A new look at the role of complement circulating in peripheral blood and expressed in hematopoietic stem cells in the regulation of hematopoiesis
<p>Hematopoietic transplantation is performed by intravenous infusion of donor-derived or autologous hematopoietic stem progenitor cells (HSPCs), which, in response to bone marrow (BM)-expressed chemoattractant navigate and home to BM hematopoietic niches. This process is followed by their engraftment and expansion to repopulate the recipient’s BM myeloablated before transplantation. The most important BM chemoattractant is the alpha-chemokine stromal-derived factor 1 (SDF-1). However, its homing role is supported by the bioactive phosphospingolipid sphingosine-1-phosphate (S1P) and by extracellular adenosine triphosphate (eATP). As we demonstrated in the past, the CXCR4 receptor for SDF-1 must be incorporated into cell surface membrane lipid rafts (MLRs) for optimal SDF-1 gradient sensing by HSPCs. Our previous research demonstrated that an important and for many years underestimated role in hematopoiesis plays an innate immunity soluble arm that is complement cascade (ComC). We provided an evidence that ComC becomes activated in BM during pharmacological mobilization in response to granulocyte colony-stimulating factor (G-CSF) or CXCR4 receptor antagonist AMD3100. In this proposal, we will focus on the role of ComC in a reverse phenomenon that is posttransplant homing/engraftment of HSPCs. It is known that the critical step before infusion of HSPCs is the myeloablative treatment of the recipient aimed to destroy pathological hematopoiesis and empty BM niches to provide space available for new transplanted HSPCs. Myeloablative treatment involves high-dose chemotherapy or myeloablative irradiation. In experimental animal transplant models, lethal irradiation is a standard procedure. The available literature indicates that both irradiation and chemotherapy induce in various organs and tissues similarly as during mobilization a state of sterile inflammation and extracellular ATP (eATP) released from damaged cells triggers this process. We postulate that the same occurs in the BM microenvironment, and in fact, our preliminary data shows that ComC becomes activated in mice after myeloablative conditioning for transplantation by lethal gamma-irradiation or exposure to myeloablative chemotherapy. It is known that ComC could be activated by i) classical-, ii) mannan-binding lectin, or iii) alternative-pathway. Activation of ComC leads to the release C3 and C5 complement components cleavage fragments - C3a and C5a anaphylatoxins that are processed by serum carboxypeptidase to desArgC3a and desArgC5a as well as leads to the formation of C5b-C9 or non-lytic or lytic membrane attack complex (MAC), which is the terminal product of ComC activation. On the other hand, both HSPCs and cells in the BM microenvironment express receptors for C3a and C5a (C3aR, C5aR1, and C5aR2). After myeloablative therapy, active ComC cleavage fragments circulate in PB. Therefore, HSPCs infused into the transplant recipient's bloodstream are exposed to these potent innate immunity mediators. This interaction of HSPCs with ComC meditators, as we propose, promotes better navigation of infused cells to the recipient BM niches and we hypothesize is a result of the promotion of MLRs formation on HSPCs. On the other hand, myeloablative conditioning for transplantation induces a state of sterile inflammation in transplant recipient BM to facilitate homing and engraftment of circulating in PB transplanted HSPCs. Finally, new intriguing evidence accumulated that in addition to the liver ComC synthesis occurs also inside some cells – e.g., in lymphocytes. Our recent data indicate that the same phenomenon occurs in HSPCs. Therefore, the intercellular expression of ComC elements known as complosome sheds new light on the underappreciated role of innate immunity in regulating hematopoiesis.</p> <p> </p> <p>This work was supported by the National Science Centre, Poland OPUS grant UMO-2022/45/B/NZ6/00475. </p> <p> </p> <p>The data included in the database were used in the following publications:</p> <p>1. <a href="https://www.nature.com/articles/s41375-024-02188-9" target="_blank" rel="noopener">https://www.nature.com/articles/s41375-024-02188-9</a></p> <p>2. <a href="https://link.springer.com/article/10.1007/s11302-023-09943-0" target="_blank" rel="noopener">https://link.springer.com/article/10.1007/s11302-023-09943-0</a></p> <p>3. <a href="https://www.nature.com/articles/s41375-023-01894-0" target="_blank" rel="noopener">https://www.nature.com/articles/s41375-023-01894-0</a></p>
Does Maitake Mushroom Extract Enhance Hematopoiesis in Myelodysplastic Patients?
ClinicalTrials.gov study NCT01099917. IPD Sharing: Not stated. Countries: 1. Publications: 0.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.