The ex vivo productionofmature neutrophils depends on the sourceofCD34+ human hematopoietic progenitors
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1143064 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30104900_1.fastq.gz | Fastqsanger.gz | |||
| SRR30104900_2.fastq.gz | Fastqsanger.gz | |||
| SRR30105000_1.fastq.gz | Fastqsanger.gz | |||
| SRR30105000_2.fastq.gz | Fastqsanger.gz | |||
| SRR30105100_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 512 |
Similar Datasets
Project description:we propose a two-stage procedure for pre-expanding hematopoietic progenitor cells and subsequent ex vivo differentiation for potential granulocyte transfusion. We compared three distinct donor sources, UCB, BM live donor, and BM deceased donor, and tested two expansion different expansion protocols. Donor sources were evaluated based on proliferation during expansion and differentiation phases, neutrophil cell yield, and function. We show that cell for cell, UCB is the most proliferative and give the greatest neutrophil yield. Further, our ex vivo-generated neutrophils of all three donor sources have an enhanced propensity for opsonin-recognizing functions relative to primary neutrophils, which may influence future treatment.
2024-11-13 | GSE273791 | GEO
Project description:Acute radiation syndrome (ARS) is a major cause of lethality following radiation disasters. A TLR5 agonist, entolimod, is among the most powerful experimental radiation countermeasures and shows efficacy in rodents and non-human primates as a prophylactic (radioprotection) and treatment (radiomitigation) modality. While the prophylactic activity of entolimod has been connected to suppression of radiation-induced apoptosis, the mechanism by which entolimod functions as a radiomitigator remains poorly understood. Here, we demonstrate that, in contrast to radioprotection, neutrophils are essential for the radiomitigative activity of entolimod. We found that neutrophils express functional TLR5 and stimulation by entolimod is a key component to the mechanism of radiomitigation. Given that the underlying effects of TLR5 agonists have been associated with NF-kB-dependent transcriptional events, we hypothesized that changes in the transcriptional profile of neutrophils post-entolimod treatment mitigates radiation damage. However, RNA sequencing data analysis showed that ex vivo stimulation of neutrophils with entolimod for 30 minutes caused changes in transcriptional profiles that were substantially weaker – both in the number of responsive genes and scale of changes – as compared with that of liver cells following in vivo entolimod treatment. These observations suggest that mitigation of radiation damage by entolimod-stimulated neutrophils involves a transcriptional-independent mechanism.
2021-09-29 | GSE179808 | GEO
Project description:In adult stomach, Lgr5 is a marker of epithelial glandular stem cells that grow in the three dimensional ex vivo culture system as organoids. However, little is known about the markers that characterize fetal progenitors before cytodifferentiation and their potential involvement in regenerative processes in adults. Using the ex vivo culture system, we isolated epithelial progenitors from the fetal stomach. These cells generated stable undifferentiated immortal spheroids showing lower growth factor requirements as compared to the adult-type gastric Lgr5-expressing organoids. Although very similar in their gene expression profiles, cultured fetal gastric and intestinal spheroids differentially expressed Sox2/Cdx2 genes involved in regional pre-patterning. Accordingly, gastric but not intestinal spheroids, spontaneously converted into the cell lineages of the adult glandular stomach ex vivo. In vivo, the Trop2 marker enriched in the fetal gastric spheroids was transiently expressed in the gastric epithelium before cytodifferentiation while it remained barely detectable under glandular homeostasis in adults. However, upon specific ablation of the Lgr5 stem cell pool, highly proliferative Trop2-expressing cells rapidly emerged in the adult epithelium, qualifying Trop2 as a marker of Lgr5-independent gastric stem cells. Together, these data indicate that the Trop2 receptor identifies gastric fetal progenitors and adult stem/progenitor cells involved in regeneration of glandular stomach.
2016-05-11 | GSE65395 | GEO
Project description:Glycogen synthase kinase-3β (GSK-3β) has been recently identified as an important regulator of stem cell function. In vitro studies show that GSK-3β inhibition delays proliferation of human haematopoietic progenitor cells while increasing numbers of late dividing multipotent progenitors. Gene expression analysis revealed that GSK-3β inhibition modulates the expression of a subset of genes that are transcriptional targets for cytokines. GSK-3β inhibition antagonised down-regulation of genes encoding cyclin dependent kinase inhibitor p57 and a member of the growth arrest and DNA damage 45 family, GADD45B as well as up-regulation of cyclin D1 by cytokines, providing a possible mechanism for the BIO-induced delay in cell cycle progression. Surprisingly, inhibition of GSK-3β earlier shown to prevent β-catenin degradation and promote the nuclear accumulation of β-catenin was not sufficient to activate its transcriptional targets in haematopoietic stem cells. GSK-3β inhibition up-regulated the expression of a several positive regulators of stem cell function suppressed during cytokine-induced proliferation. The data supports a clinical role for GSK-3β inhibition to improve engraftment efficiency of ex vivo expanded stem cells. Total RNA was isolated from three groups following expansion of CD34+ cells in cytokikes and then treatment with BIO, as described below.
2010-04-07 | E-GEOD-21073 | biostudies-arrayexpress
Project description:Epigenome and transcriptome characterization of RUNX1 deficient hematopoietic cells. We hypothesized that epigenetic alterations in key inflammatory pathway genes are acquired in RUNX1 deficient granulocyte-monocyte progenitors (GMPs) and are propagated to neutrophils. We deleted RUNX1 using Cebpa-Cre, which deletes primarily in GMPs. We analyzed the basal transcriptional changes caused by the loss of RUNX1 in purified GMPs and neutrophils by bulk RNA-seq. We evaluated if the loss of RUNX1 leads to changes in chromatin accessibility in GMPs and neutrophils by ATAC-seq. We determined that there was increased chromatin accessibility of transposable elements (TEs) in RUNX1 deficient cells. To determine if we could detect dsRNA from TEs, we pulled down dsRNA using the 9D5 antibody and performed RNA-seq. To gain insight into how RUNX1 loss affects active enhancers, we performed H3K27ac ChIP-seq on control and Runx1 deficient neutrophils. We also evaluated if RUNX1 mutations in patient neutrophils lead to changes in chromatin accessibility by ATAC-seq. We then performed Hi-C to evaluate the global high-order chromatin organization in GMPs and neutrophils. Finally, we performed RUNX1 CUT&RUN to determine RUNX1 occupancy sites in GMPs.
2023-07-12 | GSE221426 | GEO
Project description:Epigenome and transcriptome characterization of RUNX1 deficient hematopoietic cells. We hypothesized that epigenetic alterations in key inflammatory pathway genes are acquired in RUNX1 deficient granulocyte-monocyte progenitors (GMPs) and are propagated to neutrophils. We deleted RUNX1 using Cebpa-Cre, which deletes primarily in GMPs. We analyzed the basal transcriptional changes caused by the loss of RUNX1 in purified GMPs and neutrophils by bulk RNA-seq. We evaluated if the loss of RUNX1 leads to changes in chromatin accessibility in GMPs and neutrophils by ATAC-seq. We determined that there was increased chromatin accessibility of transposable elements (TEs) in RUNX1 deficient cells. To determine if we could detect dsRNA from TEs, we pulled down dsRNA using the 9D5 antibody and performed RNA-seq. To gain insight into how RUNX1 loss affects active enhancers, we performed H3K27ac ChIP-seq on control and Runx1 deficient neutrophils. We also evaluated if RUNX1 mutations in patient neutrophils lead to changes in chromatin accessibility by ATAC-seq. We then performed Hi-C to evaluate the global high-order chromatin organization in GMPs and neutrophils. Finally, we performed RUNX1 CUT&RUN to determine RUNX1 occupancy sites in GMPs.
2023-07-12 | GSE234846 | GEO
Project description:Epigenome and transcriptome characterization of RUNX1 deficient hematopoietic cells. We hypothesized that epigenetic alterations in key inflammatory pathway genes are acquired in RUNX1 deficient granulocyte-monocyte progenitors (GMPs) and are propagated to neutrophils. We deleted RUNX1 using Cebpa-Cre, which deletes primarily in GMPs. We analyzed the basal transcriptional changes caused by the loss of RUNX1 in purified GMPs and neutrophils by bulk RNA-seq. We evaluated if the loss of RUNX1 leads to changes in chromatin accessibility in GMPs and neutrophils by ATAC-seq. We determined that there was increased chromatin accessibility of transposable elements (TEs) in RUNX1 deficient cells. To determine if we could detect dsRNA from TEs, we pulled down dsRNA using the 9D5 antibody and performed RNA-seq. To gain insight into how RUNX1 loss affects active enhancers, we performed H3K27ac ChIP-seq on control and Runx1 deficient neutrophils. We also evaluated if RUNX1 mutations in patient neutrophils lead to changes in chromatin accessibility by ATAC-seq. We then performed Hi-C to evaluate the global high-order chromatin organization in GMPs and neutrophils. Finally, we performed RUNX1 CUT&RUN to determine RUNX1 occupancy sites in GMPs.
2023-07-12 | GSE221425 | GEO
Project description:Epigenome and transcriptome characterization of RUNX1 deficient hematopoietic cells. We hypothesized that epigenetic alterations in key inflammatory pathway genes are acquired in RUNX1 deficient granulocyte-monocyte progenitors (GMPs) and are propagated to neutrophils. We deleted RUNX1 using Cebpa-Cre, which deletes primarily in GMPs. We analyzed the basal transcriptional changes caused by the loss of RUNX1 in purified GMPs and neutrophils by bulk RNA-seq. We evaluated if the loss of RUNX1 leads to changes in chromatin accessibility in GMPs and neutrophils by ATAC-seq. We determined that there was increased chromatin accessibility of transposable elements (TEs) in RUNX1 deficient cells. To determine if we could detect dsRNA from TEs, we pulled down dsRNA using the 9D5 antibody and performed RNA-seq. To gain insight into how RUNX1 loss affects active enhancers, we performed H3K27ac ChIP-seq on control and Runx1 deficient neutrophils. We also evaluated if RUNX1 mutations in patient neutrophils lead to changes in chromatin accessibility by ATAC-seq. We then performed Hi-C to evaluate the global high-order chromatin organization in GMPs and neutrophils. Finally, we performed RUNX1 CUT&RUN to determine RUNX1 occupancy sites in GMPs.
2023-07-12 | GSE221422 | GEO
Project description:Epigenome and transcriptome characterization of RUNX1 deficient hematopoietic cells. We hypothesized that epigenetic alterations in key inflammatory pathway genes are acquired in RUNX1 deficient granulocyte-monocyte progenitors (GMPs) and are propagated to neutrophils. We deleted RUNX1 using Cebpa-Cre, which deletes primarily in GMPs. We analyzed the basal transcriptional changes caused by the loss of RUNX1 in purified GMPs and neutrophils by bulk RNA-seq. We evaluated if the loss of RUNX1 leads to changes in chromatin accessibility in GMPs and neutrophils by ATAC-seq. We determined that there was increased chromatin accessibility of transposable elements (TEs) in RUNX1 deficient cells. To determine if we could detect dsRNA from TEs, we pulled down dsRNA using the 9D5 antibody and performed RNA-seq. To gain insight into how RUNX1 loss affects active enhancers, we performed H3K27ac ChIP-seq on control and Runx1 deficient neutrophils. We also evaluated if RUNX1 mutations in patient neutrophils lead to changes in chromatin accessibility by ATAC-seq. We then performed Hi-C to evaluate the global high-order chromatin organization in GMPs and neutrophils. Finally, we performed RUNX1 CUT&RUN to determine RUNX1 occupancy sites in GMPs.
2023-07-12 | GSE234847 | GEO
Project description:BLUEPRINT hematopoietic progenitors
| PRJNA343828 | ENA