Transcription profiling by array of C. elegans exposed to quercetin and tannic acid
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
SUBMITTER: Stephen Sturzenbaum
PROVIDER: E-GEOD-35354 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Meta-Analysis of Global Transcriptomics Suggests that Conserved Genetic Pathways are Responsible for Quercetin and Tannic Acid Mediated Longevity in C. elegans.
Pietsch Kerstin K Saul Nadine N Swain Suresh C SC Menzel Ralph R Steinberg Christian E W CE Stürzenbaum Stephen R SR
Frontiers in genetics 20120405
Recent research has highlighted that the polyphenols Quercetin and Tannic acid are capable of extending the lifespan of Caenorhabditis elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to three concentrations of Quercetin or Tannic acid, respectively. By means of an intricate meta-analysis it was possible to compare the transcriptomes of polyphenol exposure to recently published datasets derived from ( ...[more]
Similar Datasets
Project description:Low concentrations of the dissolved leonardite humic acid HuminFeed® (HF) prolonged the lifespan and enhanced the thermal stress resistance of the model organism Caenorhabditis elegans. Furthermore growth was impaired and reproduction delayed, effects which have also been identified in other polyphenolic monomers, including tannic acid, rosmarinic acid, and caffeic acid. Moreover, a chemical modification of HF (HF-HQ), which increases its phenolic/quinonoid moieties, magnified the biological impact on C. elegans. To gain a deep insight into the molecular basis of these effects, we performed global transcriptomics on young adult (3 d) and old adult (11 d) nematodes exposed to two concentrations of HF and young adults (3 d) exposed to two concentrations of HF-HQ. The global transcriptome was compared in Caenorhabditis elegans mutant strain GE24, pha-1(e2123) exposed to 0, 0.2 and 2.0 mM HuminFeed® (HF) or Huminfeed-Hydroquinone (HF-HQ). Nematodes were harvested as 3 or 11 day old adults (for HF) or 3 day old adults (for HF-HQ).
2012-02-03 | E-GEOD-35360 | biostudies-arrayexpress
Project description:Recent research has highlighted that the polyphenols Quercetin (Q) and Tannic acid (TA) are capable of extending the lifespan of C. elegans. To gain a deep understanding of the underlying molecular genetics, we analyzed the global transcriptional patterns of nematodes exposed to Quercetin or Tannic acid concentrations that are non-effective (in lifespan extension), lifespan extending or toxic.
2012-02-03 | GSE35354 | GEO
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2014-11-01 | E-GEOD-57664 | biostudies-arrayexpress
Project description:Quercetin is a flavonol modifying numerous cell processes with potent antiproliferative effects on cancer cell-lines. The aim of this study was to explore by gene-array analysis the effect of quercetin on cancer-related gene expression in HepG2 cells, followed by verification with RT-PCR and analysis of the expected phenotypic changes (migration, cell cycle, cell proliferation). Quercetin induces significant changes on cell-adhesion related genes, leading to reduced migratory capacity and disorganization of the actin cytoskeleton. Several genes related to DNA functions, cellular metabolism and signal-transducer activities were also modified, while an early effect on G–protein related cascades possibly via protease-activated receptor 2 and phospholipase C-?1 was identified. Cyclin-D associated events in G1 and ubiquitin-dependent degradation of cyclin-D1 were also affected, resulting in cell-cycle arrest without activation of apoptosis pathways. In conclusion quercetin (3?M) exerts its cellular effects by modifying numerous genes related to mechanisms involved in cancer initiation and promotion. HepG2 cells were serum starved for 24 hours and were then treated with serum free medium with or without quercetin (3?M). Total RNA was collected at 2, 4, 12 and 24 hours and was used for gene-array experiments.
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2014-06-01 | E-GEOD-29951 | biostudies-arrayexpress
Project description:Despite extensive studies, the fundamental mechanisms responsible for the development and progression of heart failure have not yet been fully elucidated. Recent experimental and clinical studies have suggested that reactive oxygen species (ROS) play a major pathological role. Quercetin, a major flavonoid present in the human diet, has been studied widely and its biological properties are consistent with its protective role in the cardiovascular system. However, it remains unknown whether the cardioprotective effects of quercetin may also occur through the modulation of genes involved in cell survival. This study was therefore designed to examine the gene expression profiling of cultured rat primary cardiomyocytes supplemented with quercetin using DNA-microarrays and relating these data to functional effects. Experiment Overall Design: Primary heart cell cultures were obtained by isolation of cardiomyocytes from the ventricles of 2â4 day old Wistar rats and grown until complete confluence. In some dishes, 30 μM quercetin was added to the culture medium for 6, 12 or 24 h. Total RNA was extracted using Total RNA Isolation Mini Kit (Agilent Technologies, Palo Alto, CA), following the manufacturerâs protocol. The yield and purity of the RNA were measured using NanoDrop ND-1000 Spectrophotometer (NanoDrop Technologies, Inc., Rockland, Del, USA). The 28s and 18s ribosomal bands were checked using Agilent 2100 bioanalyzer with an RNA 6000 Nano LabChip Kit. For each sample, mRNA was amplified starting from 1.5 μg of totRNA by Amino Allyl MessageAmp I aRNA Kit (Ambion Inc.) to obtain amino allyl antisense RNA (aaRNA). Labeling of aaRNA was performed using NHS ester Cy3 or Cy5 dies (Amersham Biosciences, Piscataway, NJ - USA). One hybridization to Agilent 22K-gene arrays (Rat oligo array G4130A) was performed to compare quercetin supplemented cells versus unsupplemented ones. Each analysis was replicated swapping the labeling with the two cyanine dyes.
2008-05-07 | E-GEOD-7222 | biostudies-arrayexpress
Project description:To determine the effect of consumption of a quercetin-rich diet on obesity and dysregulated hepatic gene expression, C56BL/6J mice were fed for 20 weeks on control or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Chronic dietary intake of quercetin reduced body weight gain and visceral and liver fat accumulation, and improved hyperglyceamia, hyperinsulinaemia, dyslipidaemia in mice fed a Western-style diet. Feeding a Western-style diet altered expression of genes related to inflammatory responses, lipid metabolism and oxidative phosphorylation in C57BL/6J mice after 20 weeks. The results from exhaustive gene expression analysis showed that quercetin minimally influenced hepatic gene expression in mice fed the Western diet. The gene screening results (GSEA) were consistent with the notion that it did improve mitochondrial function to some extent. Quantitative RT-PCR analysis indicated that quercetin did influence important regulators of fat accumulation and metabolic disorders. Our results suggest that quercetin reduces fat accumulation presumably through decreasing oxidative stress and increasing PPARα expression, and the following improvement of gene expression related to steatosis in the liver. C56BL/6J mice were fed for 20 weeks on AIN93G (con) or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin for 20 weeks.
2012-05-29 | E-GEOD-38141 | biostudies-arrayexpress
Project description:The aim was to investigate mechanisms contributing to quercetinâs previously described effects on cell-proliferation and -differentiation, which contradicted its proposed anti-carcinogenic potency. In a 10-day experiment, 40 µM quercetin stabilized by 1mM ascorbate reduced Caco-2 differentiation up to 50% (P<0.001). Caco-2 RNA from days 5 and 10, hybridized on HG-U133A2.0 Affymetrix® GeneChips®, showed 1,743 affected genes on both days (P<0.01). All 14 Caco-2 differentiation-associated genes showed decreased expression (P<0.01), including intestinal alkaline phosphatase that was confirmed technically (qRT-PCR) and functionally (enzyme-activity). The 1,743 genes contributed to 27 affected pathways (P<0.05) categorized under 6 gene ontology (GO) processes, including apoptosis and cell-cycle. Genes within these GO-processes showed fold changes that suggest increased cell-survival and -proliferation. Furthermore, quercetin downregulated expression of genes involved in tumor-suppression and phase II metabolism, and upregulated oncogenes. Gene expression changes mediated by ascorbate-stabilized quercetin were concordant with those occurring in human colorectal carcinogenesis (â 80-90%), but were opposite to those previously described for Caco-2 cells exposed to quercetin in the absence of ascorbate (â 75-90%). In conclusion, gene expression among Caco-2 cells exposed to ascorbate-stabilized quercetin showed mechanisms contrary to what is expected for a cancer-preventive agent. Whether this unexpected in vitro effect is relevant in vivo, remains to be elucidated. Experiment Overall Design: Caco-2 cells were harvested on days 5 and 10 post-confluency. Per day, fold changes were calculated as quercetin vs. control.
2008-06-15 | E-GEOD-7259 | biostudies-arrayexpress
Project description:We examined the effect of quercetin on the gene expression and function of epididymal adipose tissue (EAT) in Western diet-induced obese mice. Quercetin suppressed the increase in the number of macrophages and the decrease in the ratio of CD4+ to CD8+ T cells in EAT, and the elevation of plasma leptin and TNFα levels in mice fed the Western diet. Comprehensive gene expression analysis revealed that quercetin suppressed gene expression associated with the accumulation and activation of immune cells, including macrophages and lymphocytes in EAT. It also improved the expression of the oxidative stress-sensitive transcription factor NFκB, NADPH oxidases, and antioxidant enzymes. Quercetin markedly increased gene expression associated with mitochondrial oxidative phosphorylation and mitochondrial DNA Quercetin most likely universally suppresses the accumulation and activation of immune cells, including anti-inflammatory cells, whereas it specifically increased gene expression associated with mitochondrial oxidative phosphorylation. Suppression of oxidative stress and NFκB activity likely contributed to the prevention of the accumulation and activation of immune cells and resulting chronic inflammation. Quercetin most likely universally suppresses the accumulation and activation of immune cells, including anti-inflammatory cells, whereas it specifically increased gene expression associated with mitochondrial oxidative phosphorylation. Suppression of oxidative stress and NFκB activity likely contributed to the prevention of the accumulation and activation of immune cells and resulting chronic inflammation. C57BL/6J mice were fed a control diet; a Western diet high in fat, cholesterol, and sucrose; or the same Western diet containing 0.05% quercetin for 18 weeks.
2016-02-25 | E-GEOD-71367 | biostudies-arrayexpress