Intervention with metabolites emulating endogenous cell transitions accelerates muscle regeneration in young and aged mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA608752 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11182032.fastq.gz | Fastqsanger.gz | |||
| SRR11182033.fastq.gz | Fastqsanger.gz | |||
| SRR11182034.fastq.gz | Fastqsanger.gz | |||
| SRR11182035.fastq.gz | Fastqsanger.gz | |||
| SRR11182036.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 66 |
Similar Datasets
Project description:Tissue regeneration following an injury requires dynamic cell-state transitions that allow for establishing the cell identities required for the restoration of tissue homeostasis and function. Here, we present a biochemical intervention that induces an intermediate cell state mirroring a transition identified during normal differentiation of myoblasts and other multipotent and pluripotent cells to mature cells. When applied in somatic differentiated cells, the intervention, composed of one-carbon metabolites, reduces some dedifferentiation markers without losing the lineage identity, thus inducing limited reprogramming into a more flexible cell state. Moreover, the intervention enabled accelerated repair after muscle injury in young and aged mice. Overall, our study uncovers a conserved biochemical transitional phase that enhances cellular plasticity in vivo and hints at potential and scalable biochemical interventions of use in regenerative medicine and rejuvenation interventions that may be more tractable than genetic ones.
2024-01-23 | GSE145933 | GEO
Project description:Tissue regeneration following an injury requires dynamic cell-state transitions that allow for establishing the cell identities required for the restoration of tissue homeostasis and function. Here, we present a biochemical intervention that induces an intermediate cell state mirroring a transition identified during normal differentiation of myoblasts and other multipotent and pluripotent cells to mature cells. When applied in somatic differentiated cells, the intervention, composed of one-carbon metabolites, reduces some dedifferentiation markers without losing the lineage identity, thus inducing limited reprogramming into a more flexible cell state. Moreover, the intervention enabled accelerated repair after muscle injury in young and aged mice. Overall, our study uncovers a conserved biochemical transitional phase that enhances cellular plasticity in vivo and hints at potential and scalable biochemical interventions of use in regenerative medicine and rejuvenation interventions that may be more tractable than genetic ones.
| S-EPMC10983034 | biostudies-literature
Project description:Metabolomic analyses reveal the specific array of metabolites present in a cell type or tissue at any given time. Multiple lines of evidence indicate that metabolites provide a readout of ongoing cellular functions, and changes in the metabolome correlate with specific biological processes1–4 as seen, for instance, during cellular differentiation. These changes are potentially associated with the regulation of signaling pathways and gene expression networks that are critical to alter cellular identity5–7. However, it is less clear whether specific metabolites or metabolic pathways can drive changes in cellular identity. To identify metabolites engaged with cell state transitions, we performed metabolomic analyses at the earliest stages of cellular differentiation and uncovered metabolites transiently upregulated just as the first transcriptional changes emerged. Specifically, we observed a wave of one-carbon metabolism conserved between three different multipotent stem cell types. Treatment of fully differentiated cells with these metabolites caused the loss of mature identity and transition toward progenitor-like states, thus demonstrating that the metabolome plays a causative role in initiating and modulating cell fate. Our studies reveal a metabolic intervention that can reprogram cellular phenotypes and could potentially be applied in regenerative medicine applications
2024-01-24 | GSE145932 | GEO
Project description:Metabolomic analyses reveal the specific array of metabolites present in a cell type or tissue at any given time. Multiple lines of evidence indicate that metabolites provide a readout of ongoing cellular functions, and changes in the metabolome correlate with specific biological processes1–4 as seen, for instance, during cellular differentiation. These changes are potentially associated with the regulation of signaling pathways and gene expression networks that are critical to alter cellular identity5–7. However, it is less clear whether specific metabolites or metabolic pathways can drive changes in cellular identity. To identify metabolites engaged with cell state transitions, we performed metabolomic analyses at the earliest stages of cellular differentiation and uncovered metabolites transiently upregulated just as the first transcriptional changes emerged. Specifically, we observed a wave of one-carbon metabolism conserved between three different multipotent stem cell types. Treatment of fully differentiated cells with these metabolites caused the loss of mature identity and transition toward progenitor-like states, thus demonstrating that the metabolome plays a causative role in initiating and modulating cell fate. Our studies reveal a metabolic intervention that can reprogram cellular phenotypes and could potentially be applied in regenerative medicine applications
2024-01-24 | GSE145897 | GEO
Project description:Metabolomic analyses reveal the specific array of metabolites present in a cell type or tissue at any given time. Multiple lines of evidence indicate that metabolites provide a readout of ongoing cellular functions, and changes in the metabolome correlate with specific biological processes1–4 as seen, for instance, during cellular differentiation. These changes are potentially associated with the regulation of signaling pathways and gene expression networks that are critical to alter cellular identity5–7. However, it is less clear whether specific metabolites or metabolic pathways can drive changes in cellular identity. To identify metabolites engaged with cell state transitions, we performed metabolomic analyses at the earliest stages of cellular differentiation and uncovered metabolites transiently upregulated just as the first transcriptional changes emerged. Specifically, we observed a wave of one-carbon metabolism conserved between three different multipotent stem cell types. Treatment of fully differentiated cells with these metabolites caused the loss of mature identity and transition toward progenitor-like states, thus demonstrating that the metabolome plays a causative role in initiating and modulating cell fate. Our studies reveal a metabolic intervention that can reprogram cellular phenotypes and could potentially be applied in regenerative medicine applications
2024-01-24 | GSE155193 | GEO
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:Gut microbiome composition after spices intervention
| PRJEB35853 | ENA
Project description:Cellular metabolism controls gene expression through allosteric interactions between metabolites and transcription factors. Methods to detect these regulatory interactions are mostly based on in vitro binding assays, but there are no methods to identify them at a genome-scale in vivo. Here we show that dynamic transcriptome and metabolome data identify metabolites that are potential effectors of transcription factors in E. coli. By switching the culture conditions between starvation and growth for 20 hours, we induced strong metabolite concentration changes and accompanying gene expression changes, which were measured by LC-MS/MS and RNA sequencing. From the transcriptome data we calculated the activity of 209 transcriptional regulators with Network Component Analysis, and then tested which metabolites correlated with these activities. This approach captured, for instance, the in vivo Hill-kinetics of CRP regulation by cyclic-AMP, a canonical example of allosteric transcription factor regulation in E. coli. By testing correlations between all pairs of transcription factors and metabolites, we predicted putative effectors of 65 transcription factors, and validated five of them in vitro. These results show that the combination of transcriptomics and metabolomics can generate hypotheses about metabolism-transcription interactions that are relevant in vivo and drive transitions between physiological states.
2019-05-31 | GSE131992 | GEO
Project description:Time-restricted feeding improves metabolic health independently of dietary macronutrient composition or energy restriction. To understand the mechanisms underpinning the effects of time-restricted feeding, we investigated the metabolic and transcriptomic profile of skeletal muscle and serum samples from 11 overweight/obese men. In muscle, 4-10% of transcripts and 14% of metabolites were periodic, with the amplitude of the metabolites lower after time-restricted feeding. Core clock genes were unaltered by either intervention, while time-restricted feeding induced rhythmicity of genes related to lipid and amino acid transport. In serum, 49-65% of the metabolites had diurnal rhythms across both conditions, with the majority being lipids. Time-restricted feeding shifted the skeletal muscle metabolite profile from predominantly lipids to amino acids. Our results show time-restricted feeding differentially affects the amplitudes and rhythmicity of serum and skeletal muscle metabolites, and regulates the rhythmicity of genes controlling lipid and amino acid transport, without perturbing the core clock.
2020-07-10 | GSE129843 | GEO
Project description:ANT2 accelerates cutaneous wound healing in aged skin by reverse senescence
| PRJNA849413 | ENA