Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA101159 | ENA |
REPOSITORIES: ENA
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Project description:Efficient bone marrow homing is a prerequisite for successful engraftment of transplanted HSPC. This study aims at determining factors important in homing of these cells from the blood to the marrow and their re-engraftment. We have isolated nucleated cells from mobilized peripheral blood stem cell harvests (PBSC). CD34+ hematopoietic stem and progenitor cells (HSPC) were enriched from PBSC harvests by immunomagnetic separation using negative selection method. Enriched cells were cultured in vitro for expansion in presence or absence of cytokine (GF: SCF+TPO+FLT3L) and/or chemokine (homing factor SDF1) mixture for 8 days at 370C in humidified atmosphere of 5% CO2 in air. GF+SDF1 –stimulated HSPC showed significantly increased total nucleated ells as well as CD34+ cells as compared to GF-stimulated HSPC as well s unstimulated cultured HSPC. On transplantation of these cells in vivo in mice model who were previously irradiated at sublethal dose of 375cGy, it was observed that GF+SDF1-stimulated HSPC exhibited significantly better engraftment in terms of presence of human CD45+ cells in mouse blood at 6 week post –transplantation. We have compared gene expression profiles of mobilized PBSC harvest cells, enriched CD34+ HSPC population and HSPC cultured in plain media, in presence with GF and in presence of GF+SDF1 derived from mobilized PBSC harvests with respect to genes involved in homing and engraftment capacities.
2016-12-11 | GSE37334 | GEO
Project description:A prospective randomized trial has shown that there is a survival advantage for allogeneic transplant patients receiving Granulocyte Colony Stimulating Factor (G-CSF) stimulated peripheral blood mononuclear cells (GPBMC) versus bone marrow (BM) as a source of stem cells. The biological basis for this advantage is not clear, and may be attributable to qualitative as well as quantitative differences in the CD34 cells, T-cells and/or the monocytes transplanted. To begin to address this issue, gene expression patterns in monocytes isolated from G-CSF mobilized peripheral blood were compared those from normal, non-mobilized peripheral blood to identify functional pathways that may distinguish these two populations. Keywords: Cell type comparison
2005-10-25 | GSE3464 | GEO
Project description:The label-free quantitative proteome was generated for 30 primary AML patient samples enriched for CD34+ cells or CKIT+ cells in the case of NPMcyt samples. As controls 3 mobilized peripheral blood CD34+ cells were included.
2025-01-07 | PXD030487 | Pride
Project description:AML1-ETO transduced human cord blood cells, CD34 selected, compared to normal cord blood cells, CD34 selected
| PRJNA100827 | ENA
Project description:Human naive T cells from peripheral blood were cultured in 24 wells coated with anti-CD3 and anti-CD28 antibodies in the presence or absence of retinoid acid, IL-12, and 1,25 (OH)2 vitamin D3. The T cells were FACS-sorted based on expression of CD3, integrin alpha4beta7, cutaneous lymphocyte antigen (CLA) and chemokine receptor 10. This serie includes microarray data from stimulated T cells under indicated conditions. Keywords: Human T cell, vitamin D and A, chemokine receptor, nuclear receptor
2007-01-22 | GSE6743 | GEO
Project description:Investigation of human hematopoietic stem cells gene expression patterns originating from different stages of ontogeny including fetal blood, cord blood, bone marrow, and mobilized peripheral blood in Lin-CD34+CD38- versus Lin-CD34+CD38+ populations. Keywords: other
2006-01-17 | GSE3823 | GEO
Project description:A highly selective and non-genotoxic G9a inhibitor, RK-701 was discovered, which upregulated the mRNA level of γ-globin but not β-globin both in human erythroid cells and in mice. Using RK-701, we examined the induction of the fetal (γ-) globin protein in human erythroid cells; HUDEP-2 and human CD34+ bone marrow and peripheral blood cells.
2023-03-11 | PXD033536 | Pride
Project description:Mast cells produce a large amount of several chemokines after cross-linking of FceRI and participate in the pathogenesis of allergic diseases. The objective of this study was to comprehensively investigate FceRI-mediated chemokine induction in human mast cells and the effect of a corticosteroid (dexamethasone) and a calcineurin inhibitor (FK506). Human peripheral blood-derived mast cells were stimulated with anti-IgE antibody in the presence of dexamethasone or FK506. Expression of eight chemokines was significantly induced in mast cells by anti-IgE stimulation. Induction of CCL2, CCL7, CXCL3 and CXCL8 by anti-IgE was significantly inhibited by dexamethasone. In contrast, induction of CCL1, CCL3, CCL4 and CCL18 was significantly inhibited by FK506. Combination of dexamethasone and FK506 suppressed production of all chemokines by anti-IgE stimulation. These results suggest that corticosteroids and calcineurin inhibitors inhibit expression of distinct subsets of chemokines and a combination of these drugs almost completely suppresses the induction of all chemokine genes in human mast cells in response to FceRI-dependent stimulation. Human peripheral blood-derived mast cells were stimulated with anti-IgE antibody in the presence of dexamethasone or FK506. Gene expression profiles were evaluated using GeneChip Human Genome U133 plus 2.0 probe arrays (Affymetrix).
2009-03-12 | E-GEOD-15174 | biostudies-arrayexpress
Project description:The label-free quantitative proteome was generated for 42 primary AML patient samples enriched for CD34+ cells (or mononuclear cells in the case of NPMcyt sameples) and as controls 6 mobilized peripheral blood CD34+ cells were included. Furthermore, 6 AML cell lines were included, and also primary mesenchymal stem cells grown under normaoxia or hypoxia were included.
2022-03-15 | PXD030463 | Pride
Project description:Gray Platelet Syndrome (GPS) is an autosomal recessive bleeding disorder characterized by a lack of α-granules in platelets and progressive myelofibrosis. Rare loss of function variants in NBEAL2, a member of the family of BEACH genes, are causal of GPS. The gene is involved in fusion, fission and trafficking of vesicles and granules. Whether NBEAL2 controls the ontogeny of granules of myeloid cells remains disputed. We found that neutrophils obtained from the peripheral blood from GPS patients have a normal distribution of azurophilic granules, but show a deficiency of specific granules, as confirmed by immuno-electron microscopy and mass spectrometry proteomics analyses. In cultures from peripheral CD34+ hematopoietic stem cells (HSCs) into mature neutrophils, the time dynamics showed concordance of NBEAL2 and specific granule protein expression at transcriptional and protein level, which were discordant in neutrophils obtained GPS-HSCs. This is indicative of normal granulopoiesis in GPS and identifies NBEAL2 as an important regulator of granule release (similar to platelets) which is suggested to occur upon egress into the blood stream. Patient neutrophil functions, including production of reactive oxygen species, chemotaxis and killing of bacteria and fungi were intact. Since GPS patients do not excessively suffer from infections, the consequence of the reduced specific granule content and lack of NET formation for innate immunity remains to be explored.
2021-01-28 | PXD017784 | Pride