Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA242389 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This study uses microarray technology to examine the erythroid progenitor mRNA of patients with transfusion dependent β-thalassaemia and compare it to erythroid progenitor mRNA from healthy controls. We observed no statistical difference in gene expression between the groups following 7 days in culture. However, following 14 days in culture we observed differential expression of 161 genes. Haematopoietic cells from the peripheral blood of 6 β-thalassaemia patients and 6 healthy controls was grown in semi-solid media. After 7 and 14 days in culture cells of erythroid origin were isolated. Total RNA was isolated from these for microarray gene expression analysis
2014-10-28 | E-GEOD-62430 | biostudies-arrayexpress
Project description:This study uses microarray technology to examine the erythroid progenitor mRNA of patients with transfusion dependent ?-thalassaemia and compare it to erythroid progenitor mRNA from healthy controls. We observed no statistical difference in gene expression between the groups following 7 days in culture. However, following 14 days in culture we observed differential expression of 277 genes. Haematopoietic cells from the peripheral blood of 6 ?-thalassaemia patients and 6 healthy controls was grown in semi-solid media. After 7 and 14 days in culture cells of erythroid origin were isolated. Total RNA was isolated from these for microarray gene expression analysis
2014-10-28 | E-GEOD-56088 | biostudies-arrayexpress
Project description:This study uses microarray technology to examine the erythroid progenitor mRNA of patients with transfusion dependent β-thalassaemia and compare it to erythroid progenitor mRNA from healthy controls. We observed no statistical difference in gene expression between the groups following 7 days in culture. However, following 14 days in culture we observed differential expression of 277 genes.
2014-10-28 | GSE56088 | GEO
Project description:This study uses microarray technology to examine the erythroid progenitor mRNA of patients with transfusion dependent β-thalassaemia and compare it to erythroid progenitor mRNA from healthy controls. We observed no statistical difference in gene expression between the groups following 7 days in culture. However, following 14 days in culture we observed differential expression of 161 genes.
2014-10-28 | GSE62430 | GEO
Project description:Differential gene expression in erythroid progenitor cells from β-thalassaemia patients and healthy controls [Bioconductor/limma R analysis]
| PRJNA264083 | ENA
Project description:Reactivation of gamma-globin is considered a promising approach for the treatment of beta-thalassaemia and sickle cell disease. Therapeutic induction of gamma-globin expression is fraught with lack of suitable therapeutic targets. In order to identify new potential targets we analysed the changes in the proteome of human primary erythroid progenitor cells by treatment with decitabine, a known, yet not clinically safe, gamma-globin inducer. Significant differentially expressed proteins were identified which were involved in various biological pathways and functional categories.
2020-01-23 | PXD006889 | Pride
Project description:Our data support that following optic nerve crush injury, ocular infiltration of immune cells causes damage to the retinal vasculature and compromises the integrity of the blood-retina barrier (BRB). Functional ablation of integrin alphaM (CD11b) attenuates immune cell trafficking, protects the BRB, and strongly enhances β-glucan-elicited retinal ganglion cells axon regeneration. Here, we performed an unbiased analysis of the vitreal proteome; we harvested vitreous humor from WT and Itgam-/- mice, β-glucan treated after optic nerve injury, and used mass spectrometry-based proteomics for differential analysis of the WT and Itgam-/- vitreous proteome (label free and tandem mass tagging).
2026-08-05 | PXD045885 | Pride
Project description:The integrity of the blood–retina barrier (BRB) is crucial for phototransduction and vision, by tightly restricting transport of molecules between the blood and surrounding neuronal cells. Breakdown of the BRB leads to the development of retinal diseases. Here, we show that Netrin-1/Unc5b and Norrin/Lrp5 signaling establish a zonated endothelial cell gene expression program that controls BRB integrity. Using single-cell RNA sequencing (scRNA-seq) of postnatal BRB-competent mouse retina endothelial cells (ECs), we investigate >100 BRB genes encoding Wnt signaling components, tight junction proteins, and ion and nutrient transporters. We find that BRB gene expression is zonated across arteries, capillaries, and veins and regulated by opposing gradients of the Netrin-1 receptor Unc5b and Lrp5-β-catenin signaling between retinal arterioles and venules. Mice deficient for Ntn1 or Unc5b display more BRB leakage at the arterial end of the vasculature, while Lrp5 loss of function causes predominantly venular BRB leakage. ScRNA-seq of Ntn1 and Unc5b mutant ECs reveals down-regulated β-catenin signaling and BRB gene expression that is rescued by Ctnnb1 overactivation, along with BRB integrity. Mechanistically, we demonstrate that Netrin-1 and Norrin additively enhance β-catenin transcriptional activity and Lrp5 phosphorylation via the Discs large homologue 1 (Dlg1) scaffolding protein, and endothelial Lrp5-Unc5b function converges in protection of capillary BRB integrity. These findings explain how arteriovenous zonation is established and maintained in the BRB and reveal that BRB gene expression is regulated at the level of endothelial subtypes.
2024-12-03 | GSE282775 | GEO
Project description:<p>Methionine cycle plays critical roles in cell fate determination by shaping epigenetic landscape, yet its function in human erythropoiesis remains undefined. Here, we show that disruption of methionine metabolism by compromising key enzyme adenosylhomocysteinase (AHCY) reshapes H3K4me3 landscape, causing erythroid cell fate reprogramming. AHCY deficiency severely impaired erythroid differentiation and expansion, leading to the generation of non-erythroid lineage hematopoietic cells, including stem/progenitor cells and immune cells, as evidenced by single-cell RNA sequencing, Pseudo temporal analysis delineated a precise dedifferentiation trajectory, revealing erythroblasts transitioning back to MEPs and HSCs. Moreover, human hematopoietic system could be reconstituted in the immunodeficient NCG-X mice by transplanting AHCY deficient erythroblasts. Mechanistically, AHCY deficiency reduced global H3K4me3 levels and altered its genomic distribution, resulting in the upregulated expression of non-erythroid transcription factors and downregulated expression of erythrocyte lineage-specific transcription factors. Integrated single-cell analyses identified transitional states with diminished AHCY in the erythroblasts of acute myeloid leukemia (AML) patient. Further flow cytometry confirmed the reduced H3K4me3 level in patient derived erythroid cells. Erythroblast isolated from AML patients with reduced H3K4me3 exhibited dedifferentiation potential into progenitor-like states. Our findings reveal a metabolic-epigenetic axis governing cell fate reprogramming in human erythropoiesis and provide insights into leukemia associated anemia.</p>
2026-06-10 | MTBLS10469 | MetaboLights