Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intervention with metabolites emulating endogenous cell transitions accelerates muscle regeneration in young and aged mice

ABSTRACT: Intervention with metabolites emulating endogenous cell transitions accelerates muscle regeneration in young and aged mice

PROVIDER: PRJNA608752 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			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:

1 - 5 of 66

Similar Datasets

Intervention with metabolites emulating endogenous cell transitions accelerates muscle regeneration in young and aged mice

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

Intervention with metabolites emulating endogenous cell transitions accelerates muscle regeneration in young and aged mice.

| S-EPMC10983034 | biostudies-literature

One-carbon metabolites control cellular identity [scRNA-seq]

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

One-carbon metabolites control cellular identity [Bulk RNA-seq_myoblast]

2024-01-24 | GSE155193 | GEO

One-carbon metabolites control cellular identity [Bulk RNA-seq]

2024-01-24 | GSE145897 | GEO

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

Transcriptome profiles of neonatal mouse intestinal organoids with or without LPS sitimulation and tryptophan metabolites intervention

Project description:We performed RNA sequencing to identify the effects of tryptphan metabolites on LPS-stimulated intestinal fibroblast.

2025-05-13 | GSE279880 | GEO

Transcriptome profiles of neonatal mouse intestinal organoids with or without LPS sitimulation and tryptophan metabolites intervention

Project description:Transcriptome profiles of neonatal mouse intestinal organoids with or without LPS sitimulation and tryptophan metabolites intervention

| PRJNA1175034 | ENA

Transcriptome profiles of RAW264.7 cells under fibroblast coculture with or without LPS sitimulation and tryptophan metabolites intervention

Project description:We performed RNA sequencing to identify the role of fibroblast in the effects of tryptphan metabolites on LPS-stimulated RAW264.7 cells.

2025-05-13 | GSE279383 | GEO

Transcriptome profiles of neonatal intestinal organoids under fibroblast coculture with or without LPS sitimulation and tryptophan metabolites intervention

Project description:We performed RNA sequencing to identify the role of fibroblast in the effects of tryptphan metabolites on LPS-stimulated mouse neonatal intestinal organoids.

2025-05-13 | GSE279881 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data