Spermidine Induces Cytoprotective Autophagy of Female Germline Stem Cell in vitro
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ABSTRACT:
PROVIDER: PRJNA690514 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13376679_1.fastq.gz | Fastqsanger.gz | |||
| SRR13376679_2.fastq.gz | Fastqsanger.gz | |||
| SRR13376680_1.fastq.gz | Fastqsanger.gz | |||
| SRR13376680_2.fastq.gz | Fastqsanger.gz | |||
| SRR13376681_1.fastq.gz | Fastqsanger.gz |
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Project description:To uncover the mechanism of SPD-induced autophagy in FGSCs, we used RNA sequencing technology to compare the mRNA expression differences between the control groups and the SPD treated groups. FGSCs mRNA profiles of the control groups and the SPD treated groups were generated by deep sequencing, in two replicates. The library quality was determined using a Bioanalyzer 2100 (Agilent). The Illumina HiSeq 2500 platform was used for RNA sequencing. The quality of RNA-seq reads was examined using FastQC.
2024-01-05 | GSE164387 | GEO
Project description:Caloric restriction and intermittent fasting prolong the lifespan and healthspan of model organisms and improve human health 1. The natural polyamine spermidine has been linked to autophagy regulation, geroprotection and reduced incidence of cardiovascular and neurodegenerative diseases across species borders 2. Here, we report that spermidine levels increase upon acute fasting in yeast, flies, mice and healthy humans. Genetic or pharmacological blockade of endogenous spermidine synthesis reduced fasting-induced autophagy in yeast, worms and human cells. Furthermore, perturbing the polyamine pathway in vivo abrogated the lifespan-extending, cardioprotective and antiarthritic effects of intermittent fasting. Mechanistically, spermidine mediated these effects via hypusination of the autophagy regulator eIF5A. In sum, the polyamine-hypusination axis thus emerges as a bona fide and phylogenetically conserved metabolic control hub for longevity and autophagy induction.
2024-04-30 | PXD035909 | Pride
Project description:Administration of spermidine, a natural polyamine whose intracellular concentration declines during human ageing, markedly extends the lifespan of various model organisms including yeast, flies and worms. In ageing yeast, spermidine treatment triggeres epigenetic deacetylation of histone H3 through inhibition of histone acetyltransferases (HAT), leading to induction of autophagy and thereby suppressing oxidative stress and necrosis. In order to further characterize the effects by spermidine supplementation of aging yeast cultures and to understand how global histone deacetylation affects gene transcription during aging, Affymetrix-based microarray analyses of three day old as well as ten day old cultures with and without administration of spermidine was performed.
2012-01-04 | E-MTAB-912 | biostudies-arrayexpress
Project description:BackgroundAutophagy is required for oogenesis and plays a critical role in response to aging caused by oxidative stress. However, there have been no reports on regulation of cytoprotective autophagy in female germline stem cells (FGSCs) in response to aging caused by oxidative stress.ResultsWe found that Spermidine (SPD) significantly increased protein expression of autophagy markers microtubule-associated protein 1 light chain 3 beta-II (MAP1LC3B-II/LC3B-II) and sequestosome-1/p62 (SQSTM1/p62), and evoked autophagic flux in FGSCs. Moreover, SPD increased the number and viability of FGSCs in vitro. Further, we found that SPD significantly reduced basal or hydrogen peroxide (H2O2)-induced up-regulated protein expression of the aging markers, cyclin dependent kinase inhibitor 2A (p16/CDKN2A) and tumor protein 53 (p53). After knockdown of p62 in FGSCs, p16 protein levels were significant higher compared with controls. However, protein p16 levels were not significantly changed in p62 knockdown FGSCs with SPD treatment compared with without SPD. Moreover, SPD significantly changed the expression of autophagy-related genes and pathways in FGSCs, as shown by bioinformatics analysis of RNA sequencing data. Additionally, SPD significantly inhibited AKT/mTOR phosphorylation.ConclusionsSPD induces cytoprotective autophagy in FGSCs in vitro and ameliorates cellular senescence of FGSCs induced by H2O2. Furthermore, SPD can ameliorate cellular senescence of FGSCs through p62. SPD might induce autophagy in FGSCs via the PI3K/Akt pathway. Our findings could be helpful for delaying aging of female germ cells due to oxidative stress and preserving female fertility.
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Project description:We use RNA-seq and ChIP-seq to explore the underlying mechanism of 028-induced autophagy in female germline stem cells in vitro
2022-08-23 | GSE136386 | GEO
Project description:Aging is associated with an increased risk of cardiovascular disease and death. Here we show that oral supplementation of the natural polyamine spermidine extends lifespan, while it exerts cardioprotective effects through reduction of cardiac hypertrophy and preservation of diastolic function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy, mitochondrial respiration and mechano-elastical properties of cardiomyocytes in vivo, coinciding with increased titin phosphorylation and suppressed subclinical inflammation. Spermidine failed to promote cardioprotection in mice lacking the autophagy-related gene Atg5 in cardiomyocytes. In Dahl salt-sensitive rats fed high-salt diet, a model for hypertension-induced congestive heart failure, spermidine reduced systemic blood pressure, increased titin phosphorylation and prevented cardiac hypertrophy and a decline in diastolic function, thus delaying the progression to heart failure. Finally, high dietary spermidine intake correlated with reduced blood pressure and a lower incidence of cardiovascular disease in humans. Our results suggest a novel and generic strategy against cardiovascular disease.
2016-11-13 | GSE86882 | GEO
Project description:Spermidine is involved in a variety of biological processes, including DNA metabolism, autophagy and aging. Previous studies have shown that spermidine can increase the percentage of mouse oocytes developing into blastocysts after in vitro fertilization. However, none of the past studies elucidated the effects of spermidine supplementation on porcine oocyte maturation. Here, we choose appropriate dose of spermidine to be added to the maturation medium during in vitro maturation (IVM) to verify whether spermidine can actively promote the maturation of porcine oocytes. Our study provided substantial evidence that spermidine exposure promoted the porcine oocyte meiotic maturation. In addition, single-cell transcriptome analysis identified the target effectors of spermidine actions in porcine oocytes, further demonstrating that spermidine exposure enhanced mitochondrial distribution and function, leading to a reduced excessive oxidative stress-induced DNA damage and early apoptosis of porcine oocytes. These findings demonstrate that spermidine not only delays ageing and cancer treatment, but also improves the quality of germ cells, which may be less likely to suffer from sterility or infertility in humans and animals.
2024-11-30 | GSE217447 | GEO
Project description:Deposition of amyloid beta (Aβ) and hyperphosphorylated tau along with glial cell-mediated neuroinflammation are prominent pathogenic hallmarks of Alzheimer’s disease (AD). In recent years, impairment of autophagy has been found to be another important feature contributing to AD progression. Therefore, the potential of the autophagy activator spermidine, a small body-endogenous polyamine often used as dietary supplement, was assessed on Aβ pathology and glial cell-mediated neuroinflammation. Oral treatment of the amyloid prone AD-like APPPS1 mice with spermidine reduced neurotoxic soluble Aβ and decreased AD-associated neuroinflammation during disease progression. Mechanistically, single nuclei sequencing revealed AD-associated microglia to be the main target of spermidine. This microglia population was characterized by increased AXL levels and expression of genes implicated in cell migration and phagocytosis. Our data highlight that the autophagy activator spermidine holds the potential to enhance Aβ degradation and to counteract glia-mediated neuroinflammation in AD pathology.
2022-07-04 | GSE206202 | GEO
Project description:Advanced age is a primary risk factor for female infertility due to reduced ovarian reserve and declining oocyte quality. However, as an important contributing factor, the role of metabolic regulation during reproductive aging is poorly understood. Here, we applied untargeted metabolomics to identify spermidine as a critical metabolite in ovaries to protect oocytes against aging. In particular, we found that spermidine level was reduced in aged ovaries and supplementation of spermidine promoted follicle development, oocyte maturation, early embryonic development and female fertility of aged mice. By micro-transcriptomic analysis, we further discovered that recovery of oocyte quality by spermidine was mediated by enhancement of mitophagy activity and mitochondrial function in aged mice, and this action mechanism was conserved in porcine oocytes under oxidative stress. Altogether, our findings demonstrate that spermidine supplementation is a potentially effective strategy to ameliorate oocyte quality and reproductive outcome of women at an advanced age.
2023-11-10 | GSE239551 | GEO
Project description:Deposition of amyloid beta (Aβ) and hyperphosphorylated tau along with glial cell-mediated neuroinflammation are prominent pathogenic hallmarks of Alzheimer’s disease (AD). In recent years, impairment of autophagy has been found to be another important feature contributing to AD progression. Therefore, the potential of the autophagy activator spermidine, a small body-endogenous polyamine often used as dietary supplement, was assessed on Aβ pathology and glial cell-mediated neuroinflammation. Oral treatment of the amyloid prone AD-like APPPS1 mice with spermidine reduced neurotoxic soluble Aβ and decreased AD-associated neuroinflammation. A subsequent proteome analysis of isolated microglia confirmed the anti-inflammatory and revealed cytoskeletal effects of spermidine in APPPS1 mice. Our data highlight that the autophagy activator spermidine holds the potential to enhance Aβ degradation and to counteract microglia-mediated neuroinflammation in AD pathology.
2022-07-04 | PXD034638 | Pride