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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE142757 | 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 [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 [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

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

2022-12-31 | GSE142760 | 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

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.

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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.

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PI3K/Akt/mTOR inhibitors in breast cancer.

Project description:Activation of the phosphoinositide 3 kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is common in breast cancer. There is preclinical data to support inhibition of the pathway, and phase I to III trials involving inhibitors of the pathway have been or are being conducted in solid tumors and breast cancer. Everolimus, an mTOR inhibitor, is currently approved for the treatment of hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative breast cancer. In this review, we summarise the efficacy and toxicity findings from the randomised clinical trials, with simplified guidelines on the management of potential adverse effects. Education of healthcare professionals and patients is critical for safety and compliance. While there is some clinical evidence of activity of mTOR inhibition in HR-positive and HER2-positive breast cancers, the benefits may be more pronounced in selected subsets rather than in the overall population. Further development of predictive biomarkers will be useful in the selection of patients who will benefit from inhibition of the PI3K/Akt/mTOR (PAM) pathway.

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