Systematic metabolome analysis of hematopoietic cells identified uridine as a vital anti-aging factor in hematopoiesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1005171 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25628814_1.fastq.gz | Fastqsanger.gz | |||
| SRR25628814_2.fastq.gz | Fastqsanger.gz | |||
| SRR25628815_1.fastq.gz | Fastqsanger.gz | |||
| SRR25628815_2.fastq.gz | Fastqsanger.gz | |||
| SRR25628816_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:In this study, we employed immunomagnetic enrichment and fluorescence-activated cell sorting (FACS) to isolate 15 hematopoietic cell types, over 9×108 hematopoietic cells from 200 young and 150 aged mice, ranging from HSPCs to mature blood cells. UPLC-MS/MS untargeted analysis identified about 2000 metabolites in each cell population, which contributed to define cell-specific signatures and depict aging landscape of blood cells. We further validated our findings by experimentally screening metabolites delaying senescence and identified uridine as potential regulator to rejuvenate aged HSPCs. To enable public access to our dataset, we have constructed an open-source platform (MetaB, www.XXX.com) for easy data browsing and analysis. Collectively, our study developed a solid reference benchmark for metabolic studies in hematopoietic system and provided additional clarity to the mechanisms underlying hematopoietic aging.
2024-06-01 | GSE240731 | GEO
Project description:Schistosomiasis-induced hepatic fibrosis, a consequence of egg-induced granulomatous lesions, remains untreated by current drugs. Therefore, the development of novel antifibrosis drugs is of paramount importance. Our previous study indicated that aberrant uridine concentrations play a pivotal role in schistosomiasis-induced hepatic fibrosis. This study aimed to explore the inhibitory role of uridine in schistosomiasis-induced liver fibrosis and the regulatory mechanism of uridine on hepatic stellate cell (HSC) activation. The results indicated that uridine could inhibit schistosomiasis-induced liver fibrosis in vivo and TGF-β-induced HSC activation in vitro. Molecular docking revealed a strong interaction between uridine and the adenosine receptor A1 (ADORA1) receptor. Subsequent in vitro investigations demonstrated that uridine modulated the cAMP/PKA/CREB pathway, influencing HSC adipogenic differentiation and exerting an antifibrotic effect. In addition, compared with praziquantel (PZQ) alone, combined uridine and PZQ therapy resulted in a reduced fibrotic area and improved hepatic parameters in vivo. Our study reveals the antifibrosis mechanism of the uridine molecule, which may be a promising drug for the treatment of schistosomiasis-induced liver fibrosis.
2025-04-22 | GSE289753 | GEO
Project description:Mycorrhizae, symbiotic interactions between soil fungi and tree roots, are ubiquitous in terrestrial ecosystems. The fungi contribute phosphorous, nitrogen and mobilized nutrients from organic matter in the soil and in return the fungus receives photosynthetically-derived carbohydrates. This union of plant and fungal metabolisms is the mycorrhizal metabolome. Understanding this symbiotic relationship at a molecular level provides important contributions to the understanding of forest ecosystems and global carbon cycling. We generated next generation short-read transcriptomic sequencing data from fully-formed ectomycorrhizae between Laccaria bicolor and aspen (Populus tremuloides) roots. The transcriptomic data was used to identify statistically significantly expressed gene models using a bootstrap-style approach, and these expressed genes were mapped to specific metabolic pathways. Integration of expressed genes that code for metabolic enzymes and the set of expressed membrane transporters generates a predictive model of the ectomycorrhizal metabolome. Results indicate the specific compounds glycine, glutamate, and allantoin are synthesized by L. bicolor and that these compounds or their metabolites may be used for the benefit of aspen in exchange for the photosynthetically-derived sugars fructose and glucose.The analysis illustrates an approach to generate testable biological hypotheses to investigate the complex molecular interactions that drive ectomycorrhizal symbiosis. These models are consistent with experimental environmental data and provide insight into the molecular exchange processes for organisms in this complex ecosystem. The method used here for predicting metabolomic models of mycorrhizal systems from deep RNA sequencing data can be generalized and is broadly applicable to transcriptomic data derived from complex systems. Fully formed L.bicolor::P.trichocapra mycorrhizae in duplicate
2011-03-25 | E-GEOD-28157 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE16432: MSI2 regulates hematopoiesis and accelerates leukemogenesis GSE22773: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LK and MS12-inducible) GSE22774: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LSK and LK) GSE22775: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (Leukemia cell lines) Refer to individual Series
2010-07-21 | E-GEOD-22778 | biostudies-arrayexpress
Project description:Metabolic studies at single cell level could directly define the cellular phenotype closest to physiological or disease states. However, the current single cell metabolome (SCM) study using mass spectroscopy has the difficulty to give a complete view of the metabolic activity in the cell, while the prediction of metabolism-phenotype relationship is limited by the potential inconsistency between transcriptomic and metabolic levels. Here, single-cell simultaneous metabolome and transcriptome profiling method (scMeT-seq) is developed, based on sub-picoliter sampling from the cell for the initial metabolome profiling followed by single cell transcriptome sequencing. This design does not only provide sufficient cytoplasm for SCM, but also nicely keeps the cellular viability for the accurate transcriptomic analysis in the same cell. Diverse relationships between the two omics are revealed in macrophages with the stimulation of lactate and lactate transporter (MCT1) antagonist. Moreover, we mapped metabolite states to the single-cell differentiation trajectory and gene correlation network of macrophages, which allows the unsupervised functional interpretation of metabolome. Thus, the established scMeT-seq should lead to a new perspective in metabolic research by transforming metabolomics from metabolite snapshot to functional approach.
2025-09-21 | GSE270852 | GEO
Project description:The Core Binding Factor (CBF) protein RUNX1 is a master regulator of definitive hematopoiesis, crucial for hematopoietic stem cell (HSC) emergence during ontogeny, which also plays vital roles in adult mice, in regulating the correct specification of numerous blood lineages. Akin to the other mammalian Runx genes, Runx1 has two promoters P1 (distal) and P2 (proximal) which generate distinct protein isoforms. The activities and specific relevance of these two promoters in adult hematopoiesis remain to be fully elucidated. Utilizing a dual reporter model we demonstrate here that the distal P1 promoter is broadly active in adult hematopoietic stem and progenitor cell (HSPC) populations. By contrast the activity of the proximal P2 promoter is more restricted and its upregulation, in both the immature Lineage- Sca1high cKithigh (LSK) and bipotential Pre-Megakaryocytic/Erythroid Progenitor (PreMegE) populations, coincides with a loss of erythroid specification. Accordingly the PreMegE population can be prospectively separated into âpro-erythroidâ and âpro-megakaryocyteâ populations based on Runx1 P2 activity. Comparative gene expression analyses between Runx1 P2+ and P2- populations indicated that the level of CD34 expression could substitute for P2 activity to distinguish these two cell populations in wild type (WT) bone marrow (BM). Prospective isolation of these two populations will provide the opportunity to further investigate and define the molecular mechanisms involved in megakaryocytic/erythroid (Mk/Ery) cell fate decisions. mRNA profiles of wild type (WT), Runx1 P2-hCD4+ (P2+) and Runx1 P2-hCD4- (P2-) Bone marrow Pre-Megakryocyte/Erythroid (PreMegE) progenitors were generated from young adult (12-16 weeks) mice by deep sequencing, in triplicate, using Illumina NextSeq 500.
2016-01-04 | E-GEOD-68958 | biostudies-arrayexpress
Project description:Proper control of inflammatory responses is essential for embryonic development, but the underlying mechanism is poorly understood. Here, we show that under physiological conditions, inactivation of ISG15, an inflammation amplifier, is associated with the interaction of Beclin 1 (Becn1), via its ECD domain, with STAT3 in the major fetal hematopoietic organ of mice. Conditional loss of Becn1 caused sequential dysfunction and exhaustion of fetal liver hematopoietic stem cells, leading to lethal inflammatory cell-biased hematopoiesis in the fetus. Molecularly, the absence of Becn1 resulted in the release of STAT3 from Becn1 tethering and subsequent phosphorylation and translocation to the nucleus, which in turn directly activated the transcription of ISG15 in fetal liver hematopoietic cells, coupled with increased ISGylation and production of inflammatory cytokines, whereas inactivating STAT3 reduced ISG15 transcription and inflammation but improved hematopoiesis potential, and further silencing ISG15 mitigated the above collapse in the Becn1 null hematopoietic lineage. The Becn1-STAT3-ISG15 axis remains functional in Atg5/7-disrupted fetal hematopoietic organs. These results suggest that Becn1, in an autophagy-independent manner, secures hematopoiesis and survival of the fetus by directly inhibiting STAT3-ISG15 activation to prevent cytokine storms. Our findings highlight a previously undocumented role of Becn1 in governing ISG15 to safeguard the fetus.
2025-05-07 | PXD057003 | Pride
Project description:The Role of Uridine Glucuronosyl transferase 2B28 (UGT2B28) in Prostate Cancer Progression
| PRJNA837779 | ENA
Project description:This dataset was generated with the goal of comparative study of gene expression in three brain regions and two non-neural tissues of humans, chimpanzees, macaque monkeys and mice. Using this dataset, we performed studies of gene expression and gene splicing evolution across species and search of tissue-specific gene expression and splicing patterns. We also used the gene expression information of genes encoding metabolic enzymes in this dataset to support a larger comparative study of metabolome evolution in the same set of tissues and species. 120 tissue samples of prefrontal cortex (PFC), primary visual cortex (VC), cerebellar cortex (CBC), kidney and skeletal muscle of humans, chimpanzees, macaques and mice. The data accompanies a large set of metabolite measurements of the same tissue samples. Enzyme expression was used to validate metabolite measurement variation among species.
2014-05-30 | E-GEOD-49379 | biostudies-arrayexpress