Integrated Metabolomic and Transcriptomic Profiling Reveals Novel Activation Induced Metabolic networks in Human T cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA532911 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8899910.fastq.gz | Fastqsanger.gz | |||
| SRR8899920.fastq.gz | Fastqsanger.gz | |||
| SRR8899930.fastq.gz | Fastqsanger.gz | |||
| SRR8899940.fastq.gz | Fastqsanger.gz | |||
| SRR8899950.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 356 |
Similar Datasets
Project description:The targeting of metabolic pathways is emerging as an exciting new approach for modulating immune cell function and polarization states. In this study, carbon tracing and systems biology approaches integrating metabolomic and transcriptomic profiling data were used to identify adaptations in human T cell metabolism important for fueling pro-inflammatory T cell function. Results of this study demonstrate that T cell receptor (TCR) stimulation leads to a significant increase in glucose and amino acid metabolism that trigger downstream biosynthetic processes. Specifically, increased expression of several enzymes such as CTPS1, IL4I1, and ASL results in the reprogramming of amino acid metabolism. Additionally, the strength of TCR signaling resulted in different metabolic enzymes utilized by T cells to facilitate similar biochemical endpoints. Furthermore, this study shows that cyclosporine represses the pathways involved in amino acid and glucose metabolism, providing novel insights on the immunosuppressive mechanisms of this drug. To explore the implications of the findings of this study in clinical settings, conventional immunosuppressants were tested in combination with drugs that target metabolic pathways. Results showed that such combinations increased efficacy of conventional immunosuppressants. Overall, the results of this study provide a comprehensive resource for identifying metabolic targets for novel combinatorial regimens in the treatment of intractable immune diseases.
2019-04-16 | GSE129829 | GEO
Project description:Integrated metabolomic and transcriptomic analysis reveals metabolic adaptation of rats to Abcg2/Abcb1a knockout
| PRJNA667494 | ENA
Project description:Integrated genomic, transcriptomic and metabolomic analysis reveals MDH2 mutation-induced metabolic disorder in recurrent focal segmental glomerulosclerosis
| PRJNA876261 | ENA
Project description:Diet-induced obesity (DIO) is rapidly becoming a global health problem, particularly as Westernization of emerging nations continues. Currently, one third of adult Americans are considered obese and, if current trends continue, >90% of US citizens are predicted to be affected by 2050. However, efforts to fight this epidemic have not yet produced sound solutions for prevention or treatment. Our studies reveal a balanced and chronobiological relationship between food consumption, daily variation in gut microbial evenness and function, basomedial hypothalamic circadian clock (CC) gene expression, and key hepatic metabolic regulatory networks , including CC and nuclear receptors (NR), that is are essential for metabolic homeostasis. “Western” diets high in saturated fats dramatically alter diurnal variation in microbial composition and function, which in turn lead to uncoupling of the hepatic CC and NR networks from central CC control in ways that offset the timing and types of regulatory factors directing metabolic function. These signals include microbial metabolites such as short chain fatty acids (SCFAs) and hydrogen sulfide (H2S) that can directly regulate or disrupt metabolic networks of the hepatocyte. Our study therefore provides insights into the complex and dynamic relationships between diet, gut microbes, and the host that are critical for maintenance of health. Perturbations of this constellation of processes, in this case by diet-induced dysbiosis and its metabolomic signaling, can potentially promote metabolic imbalances and disease. This knowledge opens up many possibilities for novel therapeutic and interventional strategies to treat and prevent DIO, ranging from the manipulation of gut microbial function to pharmacological targeting of host pathways to restore metabolic balance. Mice were raised under germ-free or specific pathogen-free condition, or germ-free followed by conventionization. Liver tissues were harvested for total RNA isolation and hybridization on Affymetrix microarrays
2013-12-24 | E-GEOD-53590 | biostudies-arrayexpress
Project description:Integrated Transcriptomic and Metabolomic Analyses for Circadian Disruption biomarker identification
| PRJNA1273983 | ENA
Project description:Although multiple gene and protein expression have been extensively profiled in human pulmonary arterial hypertension (PAH), the mechanism for the development and progression of pulmonary hypertension remains elusive. Analysis of the global metabolomic heterogeneity within the pulmonary vascular system leads to a better understanding of disease progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we showed unbiased metabolomic profiles of disrupted glycolysis, increased TCA cycle, and fatty acid metabolites with altered oxidation pathways in the severe human PAH lung. The results suggest that PAH has specific metabolic pathways contributing to increased ATP synthesis for the vascular remodeling process in severe pulmonary hypertension. These identified metabolites may serve as potential biomarkers for the diagnosis of severe PAH. By profiling metabolomic alterations of the PAH lung, we reveal new pathogenic mechanisms of PAH in its later stage, which may differ from the earlier stage of PAH, opening an avenue of exploration for therapeutics that target metabolic pathway alterations in the progression of PAH. Global profiles were determined in human lung tissue and compared across 11 normal and 12 severe pulmonary arterial hypertension patients. Using a combination of microarray and high-throughput liquid-and-gas-chromatography-based mass spectrometry, we showed unbiased metabolomic profiles of disrupted glycolysis, increased TCA cycle, and fatty acid metabolites with altered oxidation pathways in the severe human PAH lung.
2014-11-14 | E-GEOD-53408 | biostudies-arrayexpress
Project description:<p>The targeting of metabolic pathways is emerging as an exciting new approach for modulating immune cell function and polarization states. In this study, carbon tracing and systems biology approaches integrating metabolomic and transcriptomic profiling data were used to identify adaptations in human T cell metabolism important for fueling pro-inflammatory T cell function. Results of this study demonstrate that T cell receptor (TCR) stimulation leads to a significant increase in glucose and amino acid metabolism that trigger downstream biosynthetic processes. Specifically, increased expression of several enzymes such as CTPS1, IL4I1, and ASL results in the reprogramming of amino acid metabolism. Additionally, the strength of TCR signaling resulted in different metabolic enzymes utilized by T cells to facilitate similar biochemical endpoints. Furthermore, this study shows that cyclosporine represses the pathways involved in amino acid and glucose metabolism, providing novel insights on the immunosuppressive mechanisms of this drug. To explore the implications of the findings of this study in clinical settings, conventional immunosuppressants were tested in combination with drugs that target metabolic pathways. Results showed that such combinations increased efficacy of conventional immunosuppressants. Overall, the results of this study provide a comprehensive resource for identifying metabolic targets for novel combinatorial regimens in the treatment of intractable immune diseases.</p>
2024-04-03 | MTBLS926 | MetaboLights
Project description:Adhesive capsulitis (AC) affects 2–5% of the population worldwide. Patients with severe AC fail to regain a complete range of movement and experience years of shoulder pain. Unfortunately, the underlying mechanism of severe AC remains unclear. Here, we performed an integrated transcriptomic and metabolomic data analysis of serum and tissue samples from patients with severe AC, mild AC, and healthy controls. Pathways related to muscle development and myogenesis positively correlated with severe AC progression. Further, we identified an arginine-citrulline gene-compound network that may play a central role in severe AC. Comparing differentially regulated metabolites from tissue and serum, two phospholipids were recognized as potential serum markers for severe AC. In conclusion, this is the first comprehensive integrated -omics study on severe AC and provides insights into genes and compounds of the arginine-citrulline metabolic pathway that may be potential therapeutic targets for treating AC.
2023-05-30 | GSE190023 | GEO
Project description:Although the impact of circadian disruption is well recognized, definitive indicators and time windows for its detection are currently lacking. Here, by conducting transcriptomic, metabolomic, and integrated analysis, we comprehensively investigated the gene and metabolite changes on the 7th day after a single 6-hour phase advance jet lag in mice. Our findings revealed significant alterations during this post-jet lag window, especially in core clock genes Bmal1 and Cry1, and metabolites L-Arginine and SM(d18:1/18:1(11Z)), with notable differences at Zeitgeber Time 0 (ZT0), suggesting ZT0 as a key diagnostic time point. Additionally, we identified L-Serine as a potential biomarker for indexing circadian disruption irrespective of time points. Our study provides new insights into potential biomarkers for detecting circadian clock disruption.
2025-09-01 | GSE299370 | GEO
Project description:Mitochondrial stress arises from a variety of sources, including accumulation of mutations in mitochondrial DNA, generation of reactive oxygen species, and insufficient supplies of oxygen or fuel. Cells utilize multiple pathways to respond to mitochondrial injury, including mitophagy, mitochondrial fusion, and the integrated stress response / mitochondrial unfolded protein response. However, the integration of transcriptional and metabolic signatures of distinct types of mitochondrial stress are still not well defined. We defined how primary human fibroblasts respond to a panel of well-characterized inhibitors that target key pathways in the mitochondria, using sub-lethal doses to trigger adaptive stress responses. By combining metabolomic and transcriptomic analyses, we established integrated signatures of mitochondrial stress. We developed a tool, SQUID, to infer molecular triggers of mitochondrial dysfunction in other datasets. Using SQUID, we globally investigated mitochondrial stress in the TCGA PanCancer Atlas and identified defects in pyruvate import in IDH1 mutant glioma. Altogether, these studies provide a comprehensive resource detailing cellular stress responses that safeguard mitochondrial health.
2025-04-14 | GSE241261 | GEO