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Systematic metabolome analysis of hematopoietic cells identified uridine as a vital anti-aging factor in hematopoiesis

ABSTRACT: Systematic metabolome analysis of hematopoietic cells identified uridine as a vital anti-aging factor in hematopoiesis

PROVIDER: PRJNA1005171 | ENA |

REPOSITORIES: ENA

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			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

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Systematic metabolome analysis of hematopoietic cells identified uridine as a vital anti-aging factor in hematopoiesis

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

Uridine Modulates Gene Expression Programs During RANKL-Induced Osteoclastogenesis in RAW264.7 Cells

Project description:Uridine has been implicated in the regulation of metabolic and redox processes, yet its transcriptional effects during osteoclast differentiation remain unclear. This dataset profiles global gene expression in RAW264.7 cells under three conditions: untreated control, RANKL-induced osteoclastogenesis, and RANKL combined with uridine treatment. The results reveal uridine-responsive transcriptional changes involving osteoclast differentiation, oxidative stress regulation, and PI3K/Akt–FoxO–related pathways, providing mechanistic insight into uridine-mediated modulation of osteoclastogenesis.

2026-04-09 | GSE311708 | GEO

A Novel Combination Therapy with Uridine and Praziquantel effectively Alleviates Schistosomiasis-induced Hepatic Fibrosis through Promoting Adipogenic Differentiation

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

Uridine restores oocyte quality and mitigates female reproductive aging by inhibition of ferroptosis in mice

Project description:Advanced maternal age is a key factor in female infertility, primarily due to declines in ovarian reserve and oocyte quality. However, the metabolic mechanisms underlying reproductive aging remain unclear. Here, we show that uridine levels in the plasma and ovaries of aged mice are significantly reduced compared with young controls. Building on this, we find that uridine supplementation significantly improves meiotic maturation, fertilization, and early embryonic development of aged oocytes, both in vivo and in vitro. Further microtranscriptomic analyses reveal that uridine enhances oocyte quality by inhibiting ferroptosis and enhancing mitochondrial function. Moreover, integrating Limited Proteolysis-Small Molecule Mapping, western blot and siRNA-based functional assays, we identify that uridine binds Poly(rC)-binding protein 1, thereby suppressing ferroptosis and preserving mitochondrial function. Collectively, these findings demonstrate that uridine supplementation improves fertility in aged female mice and provide mechanistic insight into ferroptosis in oocyte aging.

2026-03-05 | PXD075265 | Pride

Leukemic hematopoiesis

Project description:Leukemic hematopoiesis

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Project description:metabolome

2026-01-11 | OEX00032764 | NODE

Mycorrhizal Metabolome: L. bicolor :: P. trichocapra

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

Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis

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

Streptomyces producing geranylated dihydrouridine (JBIR-68) and geranylated uridine (Simamycin)

Project description:Streptomyces isolates identified for producing geranylated dihydrouridine (JBIR-68) and geranylated uridine (Simamycin)

2026-02-18 | MSV000100884 | MassIVE

Single-cell simultaneous metabolome and transcriptome profiling revealing metabolite-gene correlation networ

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

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