Ontology highlight
ABSTRACT:
PROVIDER: PRJNA316310 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our early life environment has a profound influence on developing organs and tissues that impacts metabolic function, and determines health and disease susceptibility across the life-course. We show an adverse early-life exposure that causes metabolic dysfunction in adulthood reprograms active and repressive histone marks in the developing liver to accelerate acquisition of an adult epigenomic signature at specific genes and chromatin states. This epigenomic reprogramming persists long after the initial exposure, but remarkably, can remain transcriptionally- and metabolically-silent until later-life exposure to a Western-style (high fat-fructose-cholesterol) diet. These findings reveal the importance of epigenome:environment interactions across the life-course, which early in life accelerate epigenomic aging and reprogram the epigenome, and later in adulthood, can unlock metabolically restriced epigenetic reprogramming to drive metabolic dysfunction.
2020-03-11 | GSE130409 | GEO
Project description:Although it is increasingly accepted that some paternal environmental conditions can influence phenotypes in future generations, it remains unclear whether phenotypes induced in offspring represent specific responses to particular aspects of the paternal exposure history, or whether they represent a more generic response to paternal “quality of life”. To establish a paternal effect model based on a specific ligand-receptor interaction and thereby enable pharmacological interrogation of the offspring phenotype, we explored the effects of paternal nicotine administration on offspring phenotype in mouse. We show that paternal exposure to chronic nicotine induced a broad protective response to xenobiotic exposure in the next generation. This effect manifested as increased survival following an injection of toxic levels of nicotine, was specific to male offspring, and was only observed after these offspring were first acclimated to low levels of nicotine for a week. Importantly, offspring xenobiotic resistance was documented not only for toxic nicotine challenge, but also for toxic cocaine challenge, indicating that paternal nicotine exposure reprograms offspring to become broadly resistant to environmental toxins. Mechanistically, the reprogrammed state was characterized by enhanced clearance of nicotine in drug-acclimated animals, and we found that isolated hepatocytes displayed upregulation of enzymes that metabolize xenobiotics. Taken together, our data show that paternal nicotine exposure induces a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics in the environment.
2017-02-02 | GSE92240 | GEO
Project description:Five genome-wide microarrays were used to indentify gene expression in exposure to Tributyltin, Dichlorodiphenyltrichloroethane and 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin. The three environmental chemicals are persistent in environment and cause continuous toxical effects on human and aquatic life. Tetrahymena thermophila has the potential as a toxical model. The genome-wide microarray in Tetrahymena thermophila exposed to these toxicants was analyzed. First, genes differentially expressed under the treatment of each toxicant were identified and then their functions were categorized using GO enrichment analysis. The results may suggest that Tetrahymena thermophila is able to reflect different mechanism of different toxic-type toxicants which are similar to those in multicellular organisms. Regarding the complexity of TCDD effects, context likelihood of relatedness method (CLR) was applied to construct a TCDD-relevant network. General functions of the network are related to the epigenetic mechanism of TCDD. Based on the network analysis, a model of TCDD effect on T. thermophila was infered. Thus, Tetrahymena has the potential to be a good unicellular eukaryotic model for toxic mechanism research at genome level.
2011-06-30 | GSE26515 | GEO
Project description:Streptococcus pyogenes (Group A Streptococcus: GAS) is a major human pathogen that causes streptococcal pharyngitis, skin and soft-tissue infections, and life-threatening conditions such as streptococcal toxic shock syndrome (STSS). A large number of virulence-related genes are encoded on GAS genomes, which are involved in host-pathogen interaction, colonization, immune invasion, and long-term survival within hosts, causing the diverse symptoms. Here, we investigated the interaction between GAS-derived extracellular vesicles and host cells in order to reveal pathogenicity mechanisms induced by GAS infection.
2021-05-17 | PXD026040 | JPOST Repository
Project description:Our early life environment has a profound influence on developing organs and tissues that impacts metabolic function, and determines health and disease susceptibility across the life-course. We show an adverse early-life exposure that causes metabolic dysfunction in adulthood reprograms active and repressive histone marks in the developing liver to accelerate acquisition of an adult epigenomic signature at specific genes and chromatin states. This epigenomic reprogramming persists long after the initial exposure, but remarkably, can remain transcriptionally- and metabolically-silent until later-life exposure to a Western-style (high fat-fructose-cholesterol) diet. These findings reveal the importance of epigenome:environment interactions across the life-course, which early in life accelerate epigenomic aging and reprogram the epigenome, and later in adulthood, can unlock metabolically restriced epigenetic reprogramming to drive metabolic dysfunction.
2020-03-11 | GSE130434 | GEO
Project description:Small non-coding RNAs (sncRNAs) have been proposed as potential vectors of the interface between genes and environment. Here, we report that environmental conditions involving traumatic stress in early life, alter miRNA and piRNA composition in sperm of adult males in mice.
2014-04-13 | GSE50132 | GEO
Project description:The human liver cytosol stability model is used for predicting the stability of a drug in the cytosol of human liver cells, which is beneficial for identifying potential drug candidates early during the drug discovery process. If a drug compound is quickly absorbed, it may not reach the intended target in the body or become toxic. On the other hand, if a drug compound is too stable, it could accumulate and cause detrimental effects. The authors use an NCATS dataset of 1450 compounds screened in vitro in mouse and human cytosol fractions. Compounds were classified as stable (half-life > 30min) or unstable (half-life ≤ 30 min). Note that authors report the dataset was biased towards stable compounds.
Model Type: Machine learning model.
Model Relevance: Predicts probability of a compound stability due to liver cells metabolism.
Model Encoded by: Pauline (Ersilia)
Metadata Submitted in BioModels by: Zainab Ashimiyu-Abdusalam
Implementation of this model code by Ersilia is available here:
https://github.com/ersilia-os/eos9yy1
2024-04-22 | MODEL2404220005 | BioModels
Project description:Five genome-wide microarrays were used to indentify gene expression in exposure to Tributyltin, Dichlorodiphenyltrichloroethane and 2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin. The three environmental chemicals are persistent in environment and cause continuous toxical effects on human and aquatic life. Tetrahymena thermophila has the potential as a toxical model. The genome-wide microarray in Tetrahymena thermophila exposed to these toxicants was analyzed. First, genes differentially expressed under the treatment of each toxicant were identified and then their functions were categorized using GO enrichment analysis. The results may suggest that Tetrahymena thermophila is able to reflect different mechanism of different toxic-type toxicants which are similar to those in multicellular organisms. Regarding the complexity of TCDD effects, context likelihood of relatedness method (CLR) was applied to construct a TCDD-relevant network. General functions of the network are related to the epigenetic mechanism of TCDD. Based on the network analysis, a model of TCDD effect on T. thermophila was infered. Thus, Tetrahymena has the potential to be a good unicellular eukaryotic model for toxic mechanism research at genome level. Tetrahymena thermophila CU428 cells were cultured using 1XSPP, 30 degree, 100 rpm shaking, until 300,000 cells/ml. Cells at 300,000 cells/ml was incubated in SPP medium were treated. Two microarrays were used 4.02μl DMSO per ml SPP as the solvent and control; One microarray for 5 ppb TBT treatment 24 hours; One microarray for 1 ppb TCDD treatment 24 hours; One microarray for 4ppm DDT treatment for 24 hours.
2011-06-30 | E-GEOD-26515 | biostudies-arrayexpress
Project description:Halotolerant species are of interest since they occur naturally in environments with excess toxic ions. The cyanobacterium Halothece sp. PCC 7418 (hereafter referred to as Halothece) exhibits remarkable halotolerance and was used to examine stress-responsive regulatory mechanisms. The effects of salinity environment on Halothece transcriptomes were examined using RNA sequencing.
2023-05-21 | GSE213175 | GEO