JsNetSeto
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB72570 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12654644_1.fastq.gz | Fastqsanger.gz | |||
| ERR12654644_2.fastq.gz | Fastqsanger.gz | |||
| ERR12666658.fastq.gz | Fastqsanger.gz | |||
| ERR13669967_1.fastq.gz | Fastqsanger.gz | |||
| ERR13669967_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 5 |
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Project description:The erythroblastic island (EBI), composed of a central macrophage and surrounding erythroid cells, was the first hematopoietic niche discovered. The identity of EBI macrophages has thus far remained elusive. Gene expression profiles of BM F4/80+Epor-eGFP+ macrophages suggest a specialized function in supporting erythropoiesis.
2019-05-31 | GSE127980 | GEO
Project description:The erythroblastic island (EBI), composed of a central macrophage and surrounding maturing erythroblasts, is the erythroid precursor niche. Despite numerous studies, its precise composition is still unclear. Using multispectral imaging flow cytometry (IFC), in vitro island reconstitution, and single cell RNA-seq of EBI-component cells enriched by gradient sedimentation, we present evidence that CD11b+ cells present in the EBIs are neutrophil precursors specifically associated with bone marrow EBI macrophages, indicating that erythro-(myelo)-blastic islands are a site for terminal granulopoiesis as well as erythropoiesis and production of these lineages is dynamically regulated within this niche. We further demonstrate that the balance between these lineages is determined by pathophysiological conditions, favoring granulopoiesis during anemia of inflammation, or erythropoiesis after erythropoietin (Epo) stimulation. Finally, we provide the heterogeneous molecular profiling of EBI macrophages as revealed by Cellular Indexing of Transcriptome and Epitopes (CITE)-sequencing of mouse bone marrow EBIs at baseline and after Epo-stimulation in vivo. Altogether, these data demonstrate that EBIs serve a dual role as terminal erythropoiesis and granulopoiesis niches and the central macrophages adapt to the needs of stress erythropoiesis as well as granulopoiesis.
2022-07-22 | GSE196347 | GEO
Project description:The goal of this study was to understand the cause of anemia in lupus prone mice expressing humn TLR8. This was found to be due to a block in erythroblast differentiation form the CFUE to proerythroblast stage, a step that occurs within erythroblastic islands. We analyzed 19,309 bone marrow EBI cells and 4,794 spleen EBI cells that formed 22 clusters of cells. We confirmed the block in CFUE differentiation and found a defect in central macrophages that caused failure of erythroblast adherence
2023-07-19 | GSE189532 | GEO
Project description:Numerous studies have elucidated the neuroprotective effect of 6-gingerol in central nervous system diseases. However, the potential role and mechanism of 6-gingerol on early brain injury (EBI) after subarachnoid hemorrhage (SAH) remains poorly understood. Here, we report that 6-gingerol exerts a neuroprotective effect on SAH-induced EBI through the GBP2/PI3K/AKT pathway. A SAH rat model was established by injecting femoral artery blood into the cisterna magna. 6-gingerol or vehicle was injected intraperitoneally one hour post-SAH induction. We found that the neurological function score and brain edema of SAH rats were significantly improved after 6-gingerol treatment, as well as neuronal apoptosis was attenuated in SAH rats by Nissl staining assay and TUNEL assay. To further explore potential molecular mechanisms associated with 6-gingerol, RNA sequencing was implemented to investigate the differences in transcriptomes between SAH rats with and without 6-gingerol treatment; and found that the expression of guanylate-binding protein 2 (GBP2) evidently was suppressed with 6-gingerol treatment compared to vehicle group. In addition, dual immunofluorescence was also employed to investigate changes in neurons, astrocytes, and microglia after 6-gingerol treatment. The results showed that GBP2 was expressed in neurons but not astrocytes or microglia. Western blotting analysis results demonstrated that the PI3K/AKT pathway was activated in the SAH rats treated with 6-gingerol. Furthermore, recombinant GBP2 protein and LY294002 (PI3K inhibitor) treatment reversed the effects of 6-gingerol treatment in SAH rats. These results indicate that 6-gingerol suppressed the expression of GBP2 to activate the PI3K/AKT pathway, improve neurologic outcomes, reduce brain edema and neuronal apoptosis. In summary, our findings suggest that 6-gingerol could attenuate EBI post-SAH in rats, and 6-gingerol may serve as a novel candidate neuroprotective drug for SAH-induced EBI.
2022-07-26 | GSE201312 | GEO
Project description:Transcriptome sequencing of E.coli K12 in LB media in early exponential phase and transition to stationary phase ArrayExpress Release Date: 2010-09-30 Person Roles: submitter Person Last Name: Martincorena Person First Name: Inigo Person Mid Initials: Person Email: martinco@ebi.ac.uk Person Phone: Person Address: Person Affiliation: EBI
2011-02-05 | GSE24998 | GEO
Project description:ChiP-seq profiling of Drosophila melanogaster salivary glands to identify targets for NSL1 and MCRS2. ArrayExpress Release Date: 2010-04-16 Publication Title: The Nonspecific Lethal Complex Is a Transcriptional Regulator in Drosophila Publication Author List: Raja SJ, Charapitsa I, Conrad T, Vaquerizas JM, Gebhardt P, Holz H, Kadlec J, Fraterman S, Luscombe NM, Akhtar A. Person Roles: submitter Person Last Name: Vaquerizas Person First Name: Juan Person Mid Initials: M Person Email: jvaquerizas@ebi.ac.uk Person Phone: Person Address: Person Affiliation: EBI
2010-12-04 | GSE25709 | GEO
Project description:The erythroblastic island (EBI) functions as a niche where erythroblastic island macrophages (EBIMφ) are positioned within rings of erythroblasts, providing support and signals that orchestrate efficient erythropoiesis. Herein, we postulated burn injury impacts the EBI, given the nearly universal presence of anemia and inflammation in burn patients, and a divergent myeloid transcriptional signature we observed in murine bone marrow following burn injury, where G-CSF secretion increased neutrophil and monocyte transcripts but reduced EBIMφ transcripts. We utilized flow cytometry to investigate EBIMφ after imaging flow cytometry confirmed the heme induced transcription factor Spi-C as a robust marker of EBIMφ in Spicigfp/igfp mice. Two populations referred to as Spic+ macrophages and Spic+ Gr1 low monocytes possessed cell intrinsic GFP, with Spic+ macrophages distinguished by higher levels of GFP, F4/80, autofluorescence, and negligible CD115 staining compared to Gr1 low monocytes. Further, at least 50% of the Spic+ macrophages stained for CD163 while staining was negligible on Gr1 low monocytes. Since CD163 distinguished the populations and macrophage remnants could convolute flow cytometry analysis, total CD163 protein was quantified in marrow aspirates to corroborate results. Application of Spicigfp/igfp mice in studies revealed a G-CSF dependent reduction of Spic+ macrophages in post burn marrow that coincided with a loss of erythroid cells and that recombinant G-CSF alone was sufficient to reduce Spic+ macrophages in the marrow. These results provide the first evidence that burn injuries impact the EBI niche through G-CSF dependent depletion of EBIMφ and support the use of Spicigfp/igfp mice in investigation of EBIMφ.
2024-12-09 | GSE263318 | GEO
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| PRJEB72569 | ENA