Resveratrol attenuates the mitochondrial RNA-mediated cellular response to immunogenic stress
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ABSTRACT:
PROVIDER: PRJNA940666 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23693784_1.fastq.gz | Fastqsanger.gz | |||
| SRR23693784_2.fastq.gz | Fastqsanger.gz | |||
| SRR23693785_1.fastq.gz | Fastqsanger.gz | |||
| SRR23693785_2.fastq.gz | Fastqsanger.gz | |||
| SRR23693786_1.fastq.gz | Fastqsanger.gz |
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2023-05-03 | GSE226549 | GEO
Project description:The purpose of this study is to determine if Resveratrol, a nutritional supplement, shows a beneficial effect in the cellular function of normal liver cells and diseased liver cells (cancer cells) in samples of liver tissue taken during elective liver surgery. Outcomes based on 3 measures will test the hypothesis that Resveratrol when used as a nutritional supplement will 1)improve metabolic function in liver cells, 2)reduce cellular growth and proliferation of cancer cells, 3)decrease inflammation in the liver.
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Project description:Resveratrol is a naturally occurring compound that profoundly affects energy metabolism and mitochondrial function and serves as a calorie restriction mimetic, at least in animal models of obesity. Here we treated 10 healthy, obese men with placebo and 150 mg/day resveratrol in a randomized double-blind cross-over study for 30 days. Resveratrol supplementation significantly reduced sleeping- and resting metabolic rate. In muscle, resveratrol activated AMPK, increased SIRT1 and PGC-1alpha protein levels, increased citrate synthase activity, and improved muscle mitochondrial respiration on a fatty acid-derived substrate. Furthermore, resveratrol elevated intramyocellular lipid levels, and decreased intrahepatic lipid content, circulating glucose, triglycerides, alanine-aminotransferase, and inflammation markers. Systolic blood pressure dropped and HOMA index improved after resveratrol. In the postprandial state, adipose tissue lipolysis and plasma fatty acid and glycerol decreased. In conclusion, we demonstrate that 30 days of resveratrol supplementation induces profound metabolic changes in obese subjects, mimicking the effects of calorie restriction. double-blind randomized cross-over study, Expression profiling by microarray
2011-11-08 | E-GEOD-32357 | biostudies-arrayexpress
Project description:Resveratrol is a naturally occurring compound that profoundly affects energy metabolism and mitochondrial function and serves as a calorie restriction mimetic, at least in animal models of obesity. Here we treated 10 healthy, obese men with placebo and 150 mg/day resveratrol in a randomized double-blind cross-over study for 30 days. Resveratrol supplementation significantly reduced sleeping- and resting metabolic rate. In muscle, resveratrol activated AMPK, increased SIRT1 and PGC-1alpha protein levels, increased citrate synthase activity, and improved muscle mitochondrial respiration on a fatty acid-derived substrate. Furthermore, resveratrol elevated intramyocellular lipid levels, and decreased intrahepatic lipid content, circulating glucose, triglycerides, alanine-aminotransferase, and inflammation markers. Systolic blood pressure dropped and HOMA index improved after resveratrol. In the postprandial state, adipose tissue lipolysis and plasma fatty acid and glycerol decreased. In conclusion, we demonstrate that 30 days of resveratrol supplementation induces profound metabolic changes in obese subjects, mimicking the effects of calorie restriction.
2011-11-08 | GSE32357 | GEO
Project description:DallePazze2014 - Cellular senescene-induced
mitochondrial dysfunction
This model is described in the article:
Dynamic modelling of
pathways to cellular senescence reveals strategies for targeted
interventions.
Dalle Pezze P, Nelson G, Otten EG,
Korolchuk VI, Kirkwood TB, von Zglinicki T, Shanley DP.
PLoS Comput. Biol. 2014 Aug; 10(8):
e1003728
Abstract:
Cellular senescence, a state of irreversible cell cycle
arrest, is thought to help protect an organism from cancer, yet
also contributes to ageing. The changes which occur in
senescence are controlled by networks of multiple signalling
and feedback pathways at the cellular level, and the interplay
between these is difficult to predict and understand. To
unravel the intrinsic challenges of understanding such a highly
networked system, we have taken a systems biology approach to
cellular senescence. We report a detailed analysis of
senescence signalling via DNA damage, insulin-TOR, FoxO3a
transcription factors, oxidative stress response, mitochondrial
regulation and mitophagy. We show in silico and in vitro that
inhibition of reactive oxygen species can prevent loss of
mitochondrial membrane potential, whilst inhibition of mTOR
shows a partial rescue of mitochondrial mass changes during
establishment of senescence. Dual inhibition of ROS and mTOR in
vitro confirmed computational model predictions that it was
possible to further reduce senescence-induced mitochondrial
dysfunction and DNA double-strand breaks. However, these
interventions were unable to abrogate the senescence-induced
mitochondrial dysfunction completely, and we identified
decreased mitochondrial fission as the potential driving force
for increased mitochondrial mass via prevention of mitophagy.
Dynamic sensitivity analysis of the model showed the network
stabilised at a new late state of cellular senescence. This was
characterised by poor network sensitivity, high signalling
noise, low cellular energy, high inflammation and permanent
cell cycle arrest suggesting an unsatisfactory outcome for
treatments aiming to delay or reverse cellular senescence at
late time points. Combinatorial targeted interventions are
therefore possible for intervening in the cellular pathway to
senescence, but in the cases identified here, are only capable
of delaying senescence onset.
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2024-09-02 | BIOMD0000000582 | BioModels
Project description:Resveratrol, a natural phytoestrogen found in red wine and a variety of plants, is reported to have protective effects against lung cancer, however there is very little work directed towards the understanding of the mechanism of action of resveratrol in lung cancer. In this study we used an experimental approach to understand the biological activity and molecular mechanisms of resveratrol in A549 lung cancer cells. Gene expression profiles were compiled using an oligonucleotide microarray to determine altered expression levels in resveratrol treated cells. Keywords: Genetic modification of A549 cells in response to resveratrol
2007-09-15 | GSE9008 | GEO
Project description:Two long serial analysis of gene expression (LongSAGE) libraries of germinating conidia of Botrytis cinerea were generated with and without resveratrol treatments for unraveling the antifungal mechanisms of this phytoalexin by global transcriptome analysis – 82,786 total tags and a minimum of 15,665 unitags were obtained respectively. By tag-to-gene mapping, about 55% of the total unitags were matched to known genes. There were 109 unitags that showed significant differences in the two LongSAGE libraries, corresponding to 43 up- and 44 down-regulated genes, and 22 unmatched unitags as new gene candidates. These results showed that resveratrol inhibited expression of genes related to the glycolysis-Krebs cycle and mitochondrial electron transport chains at multiple sites in conidia germination, with induction of modified Entner–Doudoroff pathway as metabolic compensation. The chaperone-mediated protein folding and ubiquitin proteolysis systems were inhibited, while detoxification of resveratrol via ABC transporters was activated in this fungal pathogen. Keywords: Botrytis cinerea; LongSAGE; metabolic pathway; resveratrol; transcriptome
2010-04-06 | GSE11090 | GEO
Project description:Resveratrol (3,5,4'-trihydroxystilbene) extends the lifespan of diverse species including yeast, worms, and flies. In these organisms, lifespan extension is dependent on Sir2, a conserved deacetylase proposed to underlie the beneficial effects of caloric restriction (CR). Here we show that resveratrol shifts the physiology of middle-aged mice on a high-calorie diet towards that of mice on a standard diet and significantly increases their survival. Resveratrol produces changes associated with longer lifespan including increased insulin sensitivity, reduced IGF-1, increased AMPK and PGC-1α activity, increased mitochondrial number, and improved motor function. Parametric analysis of gene set enrichment (PAGE) revealed that resveratrol opposed the effects of the high-calorie diet in 144 out of 153 significantly altered pathways. These data show that improving general health in mammals using small molecules is an attainable goal and point to new approaches for treating obesity-related disorders and diseases of ageing. Keywords: Drug treatment
2006-11-03 | GSE6089 | GEO
Project description:Resveratrol is a natural product that has gained tremendous interest due to multiple reported health-beneficial effects. However, the underlying mechanisms of action of this compound remained largely controversial. Here, we demonstrate that major biological effects of resveratrol might be attributed to its bicarbonate-induced production of phenolic radicals and reactive oxygen species (ROS) such as superoxide and hydrogen peroxide under physiologically relevant conditions. These products derived from low hormetic micromolar concentrations of resveratrol led to gene expression reprogramming, which was mainly controlled by the redox-sensitive transcription factor nuclear factor (erythroid-derived 2) like 2 (Nrf2), whereas too high concentrations of resveratrol became detrimental for cells. Gentle but significant activation of Nrf2-controlled gene expression resulted in a metabolic switch and reduced cellular redox environment. Thereby cells could be preconditioned against stress, for example to protect primary keratinocytes of the human epidermis from oxidative stress that was induced by metabolization of ethanol. Hormetic shifting of cells by chemical triggers such as resveratrol towards a more reductive state might represent a powerful conceptual framework to improve cellular fitness at low nontoxic concentrations.
2015-12-31 | GSE72119 | GEO