Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Impact of partial reprogramming, aging, and differentiation on primary neural stem cells

ABSTRACT: Impact of partial reprogramming, aging, and differentiation on primary neural stem cells

PROVIDER: PRJNA1028113 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26385100_1.fastq.gz	Fastqsanger.gz
	SRR26385100_2.fastq.gz	Fastqsanger.gz
	SRR26385200_1.fastq.gz	Fastqsanger.gz
	SRR26385200_2.fastq.gz	Fastqsanger.gz
	SRR26385101_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 390

Similar Datasets

Impact of partial reprogramming, aging, and differentiation on primary neural stem cells

Project description:Partial reprogramming is of interest as a potential strategy to improve or erase aging hallmarks. The mechanisms underlying its effect on specific cell types remain unknown. Here, we investigate early transcriptional changes that could mediate the effects of reprogramming on old neural stem cells (NSCs) and their differentiation.

2024-02-04 | GSE245385 | GEO

Partial pluripotent reprogramming in C2C12 myoblasts

Project description:Partial pluripotent reprogramming has been reported to reverse some features of aging in mammalian cells and tissues. However, the impact of partial reprogramming on somatic cell identity programs and the necessity of individual pluripotency factors remain unknown. Here, we mapped trajectories of partial reprogramming in young and aged cells from multiple murine cell types using single cell transcriptomics to address these questions. We found that partial reprogramming restored youthful gene expression in adipogenic cells and mesenchymal stem cells but also temporarily suppressed somatic cell identity programs. We further screened Yamanaka Factor subsets and found that many combinations had an impact on aging gene expression and suppressed somatic identity, but that these effects were not tightly entangled. We also found that a partial reprogramming approach inspired by amphibian regeneration restored youthful gene expression in aged myogenic cells. Our results suggest that partial pluripotent reprogramming poses a neoplastic risk, but that restoration of youthful gene expression can be achieved with alternative strategies.

2022-02-28 | GSE197437 | GEO

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (10 months; long-term treatment)

Project description:Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, long-term (10 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

2022-01-11 | GSE190985 | GEO

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (1 months; sort-term treatment)

Project description:Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, short-term (1 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

2022-01-11 | GSE190984 | GEO

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (7 months; long-term treatment)

Project description:Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, long-term (7 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

2022-01-11 | GSE190983 | GEO

In vivo partial reprogramming in 4F mice

Project description:Partial reprogramming by expression of reprogramming factors (Oct4, Sox2, Klf4 and cMyc) for short periods of time restores a youthful epigenetic signature to aging cells and extends the lifespan of a premature aging mouse model. However, the effects of longer-term partial reprogramming in physiologically aging wild-type mice are unknown. Here, we have performed various long-term partial reprogramming regimens, including different onset timings, during physiological aging in different mouse strains. n=239 tissues from mice. The study involves different conditions (treated and untreated samples) and leads to 7 groups: 1) Black6 mouse +Doxocycline 2) 4 factor mouse+1 month of Doxocycline. 3) 4F mice+7month of Dox 4) 4F+10 months of Dox 5) 4F mice which are relatively old 6) B6 mice that are relatively old 7) 4F mice which are relatively young.

2021-12-10 | GSE190665 | GEO

Multi-omics characterization of partial chemical reprogramming reveals evidence of cell rejuvenation [RNA-seq]

Project description:Partial reprogramming by cyclic short-term expression of Yamanaka factors holds promise for shifting cells to younger states and consequently delaying the onset of many diseases of aging. However, the delivery of transgenes and potential risk of teratoma formation present challenges forin vivoapplications. Recent advances include the use of cocktails of compounds to reprogram somatic cells, but the characteristics and mechanisms of partial cellular reprogramming by chemicals remain unclear. Here, we report a multi-omics characterization of partial chemical reprogramming in fibroblasts from young and aged mice. We measured the effects of partial chemical reprogramming on the epigenome, transcriptome, proteome, phosphoproteome, and metabolome. At the transcriptome, proteome, and phosphoproteome levels, we saw widescale changes induced by this treatment, with the most notable signature being an upregulation of mitochondrial oxidative phosphorylation. Furthermore, at the metabolome level, we observed a reduction in the accumulation of aging-related metabolites. Using both transcriptomic and epigenetic clock-based analyses, we show that partial chemical reprogramming reduces the biological age of mouse fibroblasts. We demonstrate that these changes have functional impacts, as evidenced by changes in cellular respiration and mitochondrial membrane potential. Taken together, these results illuminate the potential for chemical reprogramming reagents to rejuvenate aged biological systems, and warrant further investigation into adapting these approaches forin vivoage reversal.

2024-03-21 | GSE246954 | GEO

Multi-omics characterization of partial chemical reprogramming reveals evidence of cell rejuvenation [Array]

Project description:Partial reprogramming by cyclic short-term expression of Yamanaka factors holds promise for shifting cells to younger states and consequently delaying the onset of many diseases of aging. However, the delivery of transgenes and potential risk of teratoma formation present challenges for in vivo applications. Recent advances include the use of cocktails of compounds to reprogram somatic cells, but the characteristics and mechanisms of partial cellular reprogramming by chemicals remain unclear. Here, we report a multi-omics characterization of partial chemical reprogramming in fibroblasts from young and aged mice. We measured the effects of partial chemical reprogramming on the epigenome, transcriptome, proteome, phosphoproteome, and metabolome. At the transcriptome, proteome, and phosphoproteome levels, we saw widescale changes induced by this treatment, with the most notable signature being an upregulation of mitochondrial oxidative phosphorylation. Furthermore, at the metabolome level, we observed a reduction in the accumulation of aging-related metabolites. Using both transcriptomic and epigenetic clock-based analyses, we show that partial chemical reprogramming reduces the biological age of mouse fibroblasts. We demonstrate that these changes have functional impacts, as evidenced by changes in cellular respiration and mitochondrial membrane potential. Taken together, these results illuminate the potential for chemical reprogramming reagents to rejuvenate aged biological systems, and warrant further investigation into adapting these approaches for in vivo age reversal.

2024-03-21 | GSE247179 | GEO

Single-cell gene expression of the subventricular zone (SVZ) neurogenic niche after partial reprogramming

Project description:Partial reprogramming has the potential to reverse age-related decline in some tissues. Its impact on the cell types within the aging brain, particularly the subventricular zone neurogenic niche, is unknown.

2024-02-04 | GSE224438 | GEO

Initiation Phase Cellular Reprogramming Rejuvenates DNA Damage Repair Defect In The Ercc1 Accelerated Aging Mouse Model

Project description:Unlike aging somatic cells, which exhibit a decline in molecular fidelity and eventually reach a state of replicative senescence, pluripotent stem cells can indefinitely replenish themselves while retaining full homeostatic capacity. The conferment of beneficial -pluripotency related traits via in vivo partial cellular reprogramming (IVPR) significantly extends lifespan and restores aging phenotypes in mouse models. Although the phases of cellular reprogramming are well characterized, details of the rejuvenation processes are poorly defined. Here we created the first reprogrammable accelerated aging mouse model with a DNA damage repair defect to better understand the effects of reprogramming on a key driver of aging. Using enhanced partial reprogramming by combining small molecules with the Yamanaka factors, we observed potent reversion of DNA damage, significant upregulation of multiple DNA damage repair processes, and restoration of the epigenetic clock is observed. In addition, we present evidence that TGFb inhibition of the ALK5 or ALK2 receptor is able to phenocopy some benefits including epigenetic clock restoration suggesting a role in the mechanism of rejuvenation during partial reprogramming.

2023-05-11 | GSE231853 | 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