Gene expression profile of hematopoietic stem cells (CD34+ cells) with or without nanoparticles
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Sezin Aday
PROVIDER: E-GEOD-51421 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To understand the the effect of poly(lactic-co-glycolic acid) nanoparticles (NPs) encapsulating a fluorine contrast agent on human umbilical vein endothelial cells (HUVECs), we have employed whole genome microarray expression profiling. The NPs used in this study were prepared in our lab. HUVECs were ordered from Lonza (Cat# C2517A). HUVECs were incubated with NPs for 4 hours. After 4 h, the cells were washed couple of times to remove the NPs and gene expression profiles were detected after 20 h (total time: 24 h) and 7 d in the absence of NPs. HUVECs after 24 h without nanoparticles were used as controls. The gene expression in HUVECs was measured at 24 h and 7 d after incubation with nanoparticles. Three independent experiments were performed at each time.
2014-06-01 | E-GEOD-51661 | biostudies-arrayexpress
Project description:To understand the the effect of poly(lactic-co-glycolic acid) nanoparticles (NPs) encapsulating a fluorine contrast agent on hematopoietic stem cells (CD34+ fraction of umbilical cord blood mononuclear cells), we have employed whole genome microarray expr
2014-06-01 | GSE51421 | GEO
Project description:EZH2, the enzymatic component of PRC2, has been identified as a key factor in hematopoiesis. EZH2 loss of function mutations have been found in myeloproliferative neoplasms, more particularly in myelofibrosis, but the precise function of EZH2 in megakaryopoiesis is not fully delineated. Here, we show that EZH2 inhibition by small molecules and shRNA induces MK commitment by accelerating lineage marker acquisition without change in proliferation. Later in differentiation, EZH2 inhibition blocks proliferation and endomitosis and decreases proplatelet formation. EZH2 inhibitors similarly reduce polyploidization and proplatelet formation of JAK2V617F MK. In transcriptome profiling, the defect in proplatelet formation was associated with an aberrant actin cytoskeleton regulation pathway, whereas polyploidization was associated with an inhibition of expression for a set of genes involved in DNA replication and repair, and an upregulation of CDK inhibitors, more particularly CDKN1A and CDKN2D. The knockdown of CDKN1A and/or CDKN2D could partially rescue the percentage of polyploid MKs. However only CDKN1A was regulated by H3K27me3 suggesting that EZH2 controls MK polyploidization through a direct regulation of CDKN1A and indirectly of CDKN2D.
2021-11-02 | E-MTAB-8610 | biostudies-arrayexpress
Project description:EZH2, the enzymatic component of PRC2, has been identified as a key factor in hematopoiesis. EZH2 loss of function mutations have been found in myeloproliferative neoplasms, more particularly in myelofibrosis, but the precise function of EZH2 in megakaryopoiesis is not fully delineated. Here, we show that EZH2 inhibition by small molecules and shRNA induces MK commitment by accelerating lineage marker acquisition without change in proliferation. Later in differentiation, EZH2 inhibition blocks proliferation and endomitosis and decreases proplatelet formation. EZH2 inhibitors similarly reduce polyploidization and proplatelet formation of JAK2V617F MK. In transcriptome profiling, the defect in proplatelet formation was associated with an aberrant actin cytoskeleton regulation pathway, whereas polyploidization was associated with an inhibition of expression for a set of genes involved in DNA replication and repair, and an upregulation of CDK inhibitors, more particularly CDKN1A and CDKN2D. The knockdown of CDKN1A and/or CDKN2D could partially rescue the percentage of polyploid MKs. However only CDKN1A was regulated by H3K27me3 suggesting that EZH2 controls MK polyploidization through a direct regulation of CDKN1A and indirectly of CDKN2D.
2021-11-02 | E-MTAB-8609 | biostudies-arrayexpress
Project description:Histone deacetylase (HDAC) inhibitors are widely utilized in hematopoietic malignance therapy; nevertheless, little is currently known concerning their effects on normal myelopoiesis. In order to investigate a putative interference of HDAC inhibitors in myeloid commitment of hematopoietic stem/progenitor cells (HSPCs) we treated CD34+ cells with valproic acid (VPA). Moreover, we investigate changes in gene expression induced by VPA treatment on HSPCs, by means of microarray analysis in VPA treated and untreated (CTR) CD34+ cells. VPA treatment induced H4 histone acetylation in CD34+ cells and blocked them in G0-G1 phase of cell cycle. CD34 expression is maintained for a longer time in VPA treated cells, while the physiological decrease of CD34 antigen occurred in CTR cells. Moreover, VPA favored erythrocyte and megakaryocyte differentiation at the expense of granulocyte and mono-macrophage lineages, as demonstrated by immunophenotyping, morphological and clonogenic analysis. Finally, we demonstrated that VPA up-regulated master gene regulators of erythrocyte and megakaryocyte differentiation (GFI1B and MLLT3) through histone iper-acetylation of their promoters. These results indicate that VPA treatment enhances erythrocyte and megakaryocyte differentiation at the expense of granulocyte and mono-macrophage one. Microarray data provide for the first time a detailed molecular support for the biological effects promoted by VPA treatment in HSPCs. Human CD34+ cells were purified from umbilical Cord Blood (CB) samples. After an initial 24 hours of incubation, CD34+ cells were exposed to VPA. Total cellular RNA was extracted from untreated (CTR) and VPA treated CD34+ HSCs after 48 hours of treatment.
2013-04-11 | E-GEOD-31283 | biostudies-arrayexpress
Project description:Expression profiling of progenitor cells from human supraclavicular and subcutaneous adipose tissue. Studies in animal models revealed that brown and white adipocytes derive from different progenitor cells. Molecular characteristics of these cells have not been investigated in detail in humans. Results provide evidence into the molecular basis of the difference of white and brown progenitor cells in humans. Progenitor cells from paired samples of supraclavicular and subcutaneous of six patients undergoing neck surgery were isolated by collagenase digestion and subsequently transferred to cell culture. After reaching subconfluency (7 days), we harvested RNA and analyzed differencens in gene expression by microarray analysis.
2014-08-05 | E-GEOD-54280 | biostudies-arrayexpress
Project description:Leukemic stem cells (LSC) might be the source for leukemic disease self-renewal and account for disease relapse after treatment, which makes them a critical target for further therapeutic options. Leukemia associated antigens (LAA) might be suitable structures to be attacked by immunotherapeutic agents. We performed primary AML sample enrichment and microarray studies to define LAA expression levels in AML. We compared the LAA expression in the enriched CD34+CD38- AML fraction to that of enriched HSC of healthy donors and AML bulk cells (CD34+CD38+, CD34-CD38+ and CD34-CD38). Furthermore, we investigated the expression patterns of co-stimulatory molecules in LSC, bulk AML cells and enriched HSC, Conclusion: We demonstrated the differential expression of several LAA in LSC, and their suitability as target structures. We enriched primary AML samples using CD34 and CD38 as markers to compare LAA expression levels of LSC, HSC and AML bulk. LAA expression profiles comparing LSC, HSC and leukemic bulk AML citation: Leukemic progenitor cells are susceptible to targeting by stimulated cytotoxic T cells against immunogenic leukemia-associated antigens Vanessa Schneider, Lu Zhang, Markus Rojewski, Natalie Fekete, Hubert Schrezenmeier, Alexander Erle, Lars Bullinger, Susanne Hofmann, Marlies Götz, Konstanze Döhner, Susann Ihme, Hartmut Döhner, Christian Buske, Michaela Feuring-Buske, Jochen Greiner
2015-04-23 | E-GEOD-68172 | biostudies-arrayexpress
Project description:To investigate the therapeutic potential of targeting RUNX1/ETO with lipid nanoparticles encapsulating chemically modefied siRNA. Epegnomic profiling was performing on cells lines after lipid nanoparticles in vitro.
2022-11-09 | GSE217110 | GEO
Project description:To investigate the therapeutic potential of targeting RUNX1/ETO with lipid nanoparticles encapsulating chemically modefied siRNA. Chromatin Accessibility (ATAC-seq) was performing on cells lines after lipid nanoparticles in vitro.
2022-11-09 | GSE217112 | GEO
Project description:CD99 is a transmembrane protein, whose expression is constantly associated to EwingM-bM-^@M-^Ys Sarcoma (EWS), a class of pediatric bone tumors with particular poor prognosis. We previously reported that engagement of CD99 leads to massive and rapid EWS cell death through a non-canonical path. Here we report that death occurs through a novel mechanism starting from classical apoptotic features, such as phosphatydilserine exposure on cell surface and mitochondrial depolarization and ending with massive cytoplasmic hypervacuolization (autophagosomes and micropinosomes). Mechanistically, CD99 induces upregulation of IGFI-R and RAS and rapid MDM2 degradation, which leads to p53 reactivation. We propose that upon CD99 engagement and subsequent p53 reactivation, the EWS-ets oncogene becomes insufficient to sustain EWS transformation; in this context, up-regulated RAS, deprived of a cooperating oncogenic stimulus, might contribute to the delivery of fatal rather than pro-survival signal. The most CD99-responsive EWS cells have either wild type or transcriptional active P53, though mutated, and greatly benefit from MDM2 degradation. Due to the low rate of P53 inactivating mutations in EWS patients, these findings sustain CD99-targeting with specific MAbs either to directly kill EWS cells or to increase sensitivity to chemotherapy. By recruiting also RAS, CD99 delivers a signal which exceeds that of drugs designed exclusive to reactivate p53 functions, besides being easily druggable Ewing Sarcoma cell lines 6647 control or treated with the anti-CD99 0662 MAb were profiled to discover mechanisms related to CD99 targeting. Treated cells were compared to control cells after 30, 60 and 120 minutes of exposure to 0662 (10M-BM-5g/ml); all treatments are in duplicate.
2015-02-01 | E-GEOD-36097 | biostudies-arrayexpress