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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens Macaca mulatta

PROVIDER: GSE142760 | GEO | 2022/12/31

REPOSITORIES: GEO

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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

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 [human blood]

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

| PRJNA598216 | 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

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

Reducing ER stress with chaperone therapy reverses sleep fragmentation and cognitive decline in aged mice.

Project description:As the aging population grows, the need to understand age-related changes in health is vital. Two prominent behavioral changes that occur with age are disrupted sleep and impaired cognition. Sleep disruptions lead to perturbations in proteostasis and endoplasmic reticulum (ER) stress in mice. Further, consolidated sleep and protein synthesis are necessary for memory formation. With age, the molecular mechanisms that relieve cellular stress and ensure proper protein folding become less efficient. It is unclear if a causal relationship links proteostasis, sleep quality, and cognition in aging. Here, we used a mouse model of aging to determine if supplementing chaperone levels reduces ER stress and improves sleep quality and memory. We administered the chemical chaperone 4-phenyl butyrate (PBA) to aged and young mice, and monitored sleep and cognitive behavior. We found that chaperone treatment consolidates sleep and wake, and improves learning in aged mice. These data correlate with reduced ER stress in the cortex and hippocampus of aged mice. Chaperone treatment increased p-CREB, which is involved in memory formation and synaptic plasticity, in hippocampi of chaperone-treated aged mice. Hippocampal overexpression of the endogenous chaperone, binding immunoglobulin protein (BiP), improved cognition, reduced ER stress, and increased p-CREB in aged mice, suggesting that supplementing BiP levels are sufficient to restore some cognitive function. Together, these results indicate that restoring proteostasis improves sleep and cognition in a wild-type mouse model of aging. The implications of these results could have an impact on the development of therapies to improve health span across the aging population.

| S-EPMC9197403 | biostudies-literature

GDF11 Regulates PC12 Neural Stem Cells via ALK5-Dependent PI3K-Akt Signaling Pathway.

Project description:Growth differentiation factor 11 (GDF11), belonging to the transforming factor-β superfamily, regulates anterior-posterior patterning and inhibits neurogenesis during embryonic development. However, recent studies recognized GDF11 as a rejuvenating (or anti-ageing) factor to reverse age-related cardiac hypertrophy, repair injured skeletal muscle, promote cognitive function, etc. The effects of GDF11 are contradictory and the mechanism of action is still not well clarified. The objective of the present study was to investigate effects of GDF11 on PC12 neural stem cells in vitro and to reveal the underlying mechanism. We systematically assessed the effects of GDF11 on the life activities of PC12 cells. GDF11 significantly suppressed cell proliferation and migration, promoted differentiation and apoptosis, and arrested cell cycle at G2/M phase. Both TMT-based proteomic analysis and phospho-antibody microarray revealed PI3K-Akt pathway was enriched when treated with GDF11. Inhibition of ALK5 or PI3K obviously attenuated the effects of GDF11 on PC12 neural stem cells, which exerted that GDF11 regulated neural stem cells through ALK5-dependent PI3K-Akt signaling pathway. In summary, these results demonstrated GDF11 could be a negative regulator for neurogenesis via ALK5 activating PI3K-Akt pathway when it directly acted on neural stem cells.

| S-EPMC9602726 | biostudies-literature

PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours.

Project description:The present study examined the expression of mammalian target of rapamycin (mTOR) and mutations in the phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway in 54 patients with typical carcinoid tumours (TC) or atypical carcinoid tumours (AC). In total, 54 bronchopulmonary neuroendocrine tumour (NET) surgical specimens, consisting of 17 TC, 8 AC, 17 large-cell neuroendocrine carcinoma (LCNEC), and 12 small-cell lung carcinoma (SCLC) samples, were tested for mTOR by immunohistochemistry, and 104 exon sites were tested in the PI3K/AKT/mTOR pathway by nested polymerase chain reaction. It was found that the positive rates for mTOR expression in TC/AC and LCNEC/SCLC were 60 (15/25) and 55.2% (16/29), respectively. In total, 4 missense mutations were found in 3 patients with TC/AC, including mutations in exon 48 of mTOR (c.6667C>T), exon 21 of tuberous sclerosis complex (TSC) 1 (c.2765G>A), and exons 12 (c.1265C>T) and 19 (c.2148C>T) of TSC2. To the best of our knowledge, mutations in exon 48 of mTOR and exon 21 of TSC1 have not been previously reported. Tissues from patients with single mutations exhibited strong positive mTOR immunohistochemical staining, and tissues from patients with double mutations were weakly positive. The same mutations were not observed in SCLC or LCNEC. In conclusion, gene mutations were observed and an association between the gene mutations and mTOR expression were indicated in the PI3K/AKT/mTOR pathway in TC/AC tumours. Those mutations may be driver genes and treatment targets.

| S-EPMC5529984 | biostudies-other

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