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GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [human blood]

ABSTRACT: GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [human blood]

PROVIDER: PRJNA598216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10806100.fastq.gz	Fastqsanger.gz
	SRR10806101.fastq.gz	Fastqsanger.gz
	SRR10806102.fastq.gz	Fastqsanger.gz
	SRR10806103.fastq.gz	Fastqsanger.gz
	SRR10806104.fastq.gz	Fastqsanger.gz

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Similar Datasets

GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline

Project description:GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline

| PRJNA598212 | ENA

GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [mice tissue]

Project description:GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [mice tissue]

| PRJNA598215 | ENA

GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [monkey blood]

Project description:GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [monkey blood]

| PRJNA598217 | ENA

Restoring Systemic GDF11 Levels Reverses Age-Related Dysfunction in Mouse Skeletal Muscle

Project description:In this study, we investigated signaling pathways in Skeletal muscle precursors that are altered with aging and age-related deficits in muscle regenerative potential. We performed fluorescence activated cell sorting (FACS) to obtain highly purified skeletal muscle satellite cells from young, middle-aged and old mice. Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction. We used Affymetrix Mouse Genome array to identify global transcriptional changes associated with age in skeletal muscle precursors.

2014-05-08 | E-GEOD-50821 | biostudies-arrayexpress

GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-31 | GSE142760 | GEO

Restoring Systemic GDF11 Levels Reverses Age-Related Dysfunction in Mouse Skeletal Muscle

2014-05-08 | GSE50821 | GEO

GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [mice tissue]

Project description:We implemented transcriptomic analyses of different tissues of 10M and 15M mice; These mice with the treatment of rGDF11 for 30 days.

2022-12-31 | GSE142759 | GEO

GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [monkey blood]

Project description:We implemented transcriptomic analyses of blood from young and aged monkey

2022-12-31 | GSE142758 | GEO

GDF11 rejuvenates neural stem cells via Smad2/3-PI3K-AKT-mTOR and reverses aged-dependent cognitive decline [human blood]

Project description:We implemented transcriptomic analyses of blood from young and aged people

2022-12-31 | GSE142757 | GEO

Protogenin Facilitates Trunk-to-Tail HOX Code Transition via Modulating GDF11/SMAD2 Signaling in Mammalian Embryos

Project description:Vertebral axial patterning is determined during embryogenesis via complicated regulation involving multiple signaling networks. This study revealed that protogenin (Prtg), a member of the immunoglobulin superfamily, is involved in controlling vertebral patterning. Prtg knockout (Prtg-/-) mice exhibited anterior homeotic transformations in their vertebral columns accompanied by significant alternations in the expression of numerous homeobox (Hox) genes. Transcriptomic profiling of Prtg-/- embryos revealed that genes regulated by Prtg play a pivotal role in modulating axial development, displaying prominent associations with the transforming growth factor beta (TGFβ) signaling pathway. Additionally, we observed a pronounced reduction in TGFβ signaling activity in Prtg-/- embryos, as evidenced by decreased phosphorylated Smad2 (pSmad2) levels within the developing tail region. Furthermore, we introduced human induced pluripotent stem cell-derived presomitic mesoderm-like (hiPSC-PSM) cells as an in vitro model to explore the role of PRTG in somitogenesis, specifically focusing on the collinear expression of HOX genes. Our findings indicate that PRTG knockout in hiPSC-PSM cells results in delayed posterior HOX gene expression. Intriguingly, supplementation with growth differentiation factor 11 (GDF11) successfully rescued the abnormal expression of posterior HOX genes, providing compelling evidence that PRTG’s regulation of HOX genes is mediated by the GDF11/SMAD2 signaling pathway.

2024-11-13 | GSE256393 | GEO

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