Rattus norvegicus
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PROVIDER: PRJNA301798 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Assessing concordance of drug-induced transcriptional response in rodent liver and cultured hepatocytes
2020-06-16 | E-GEOD-74903 | ExpressionAtlas
Project description:Male Sprague-Dawley rats were used to establish exhausted-exercise model by motorized rodent treadmill. Yu-Ping-Feng-San at doses of 2.18 g/kg was administrated by gavage before exercise training for 10 consecutive days. Quantitative proteomics was performed for assessing the related mechanism of Yu-Ping-Feng-San.
2022-08-12 | PXD032737 | Pride
Project description:Conserved Transcriptional Response of Rodent Liver to TCDD: Rat
| PRJNA107443 | ENA
Project description:The effect of drugs, disease and other perturbations on mRNA levels are studied using gene expression microarrays or RNA-seq, with the goal of understanding molecular effects arising from the perturbation. Previous comparisons of reproducibility across laboratories have been limited in scale and focused on a single model. The use of model systems, such as cultured primary cells or cancer cell lines, assumes that mechanistic insights derived with would have been observed via in vivo studies. We examined the concordance of compound-induced transcriptional changes using data from several sources: rat liver and rat primary hepatocytes (RPH) from Drug Matrix (DM) and open TG-GATEs (TG), primary human hepatocytes (HPH) from TG, and mouse liver / HepG2 results from the Gene Expression Omnibus (GEO) repository. Gene expression changes for treatments were normalized to controls and analyzed with three methods: 1) gene level for 9071 high expression genes in rat liver, 2) gene set analysis (GSA) using canonical pathways and gene ontology sets, 3) weighted gene co-expression network analysis (WGCNA). Co-expression networks performed better than genes or GSA on a quantitative metric when comparing treatment effects within rat liver and rat vs. mouse liver. Genes and modules performed similarly at Connectivity Map-style analyses, where success at identifying similar treatments among a collection of reference profiles is the goal. Comparisons between rat liver and RPH, and those between RPH, HPH and HepG2 cells reveal low concordance for all methods. We investigate differences in the baseline state of cultured cells in the context of drug-induced perturbations in rat liver and highlight the striking similarity between toxicant-exposed cells in vivo and untreated cells in vitro. Gene expression studies in model systems are widely used for understanding the mechanism of drugs and other perturbations in biological systems. Other researchers have examined the reproducibility of microarray studies between laboratories, or comparing microarrays and/or RNA sequencing. However, no large scale studies have compared results from protocols which differ in minor details, or results generated in vivo vs. in vitro culture system thought to serve as useful models. The rat liver is by far the most extensively studied model evaluating effects of drugs and other perturbations, and existing data allowed us to assess the level of concordance between rat liver and rat primary hepatocytes cultured in collagen-coated plates (i.e. âflatâ culture) for hundreds of drugs. We found that the mouse liver serves as a better model of the rat liver than do rat primary hepatocytes, even after allowing for differences due to pharmacokinetics. The low concordance observed between rat liver and rat hepatocytes suggests that validating the utility of âomics data generated on emerging cell culture approaches (e.g. âorgan-on-a-chipâ, 3D-printed tissues) using rat cells and comparison to the rat liver may be necessary in order to gain confidence these approaches substantially improve on traditional culture models of human cells. To identify transcriptional changes in culture, rat primary hepatocytes (RPH) were isolated from three male Sprague Dawley rats. During the isolation and prior to perfusion, a lobe of liver was tied off to serve as the liver in situ reference sample. Cells were isolated and samples from the cell pellet (time zero) and cells cultured for 4, 24 and 48 hours. Three biological replicates were generated for each group (one from each rat). Each biological replicate was analyzed via 3 technical replicates, for a total of 9 array hybridizations per group.
2015-11-12 | E-GEOD-74903 | biostudies-arrayexpress
Project description:Rat Primary Cultured Hepatocytes: Control vs SQ1 or Pravastatin treatment.
| PRJNA322223 | ENA
Project description:Formaldehyde (HCHO) is the simplest form of aldehyde and it is naturally present in a wide range of resources. In spite of its cosmopolitan presence, formaldehyde can have deleterious health effects at higher concentrations like leukemia. However, most of the studies carried out so far have focused on the effect of formaldehyde exposure through inhalation and not much has been studied on the its exposure through food. In this context, the present study was carried out to investigate the effect of formaldehyde exposure through drinking water on the liver proteome of rat which would not only be helpful in assessing the impact of formaldehyde on health of organisms but also would be helpful in understanding the mechanism of detoxification.
2020-01-07 | PXD010534 | Pride
Project description:Like many per- or polyfluorinated alkyl substances (PFAS), toxicity studies with HFPO-DA (ammonium, 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)-propanoate; CASRN 62037-80-3), a short-chain PFAS used in the manufacture of some types of fluorinated polymers, indicate that the liver is the primary target of toxicity in rodents following oral exposure. Although the current weight of evidence supports the PPARa mode of action (MOA) for liver effects in HFPO-DA-exposed mice, alternate MOAs have also been hypothesized including PPARg or cytotoxicity. To further evaluate the MOA for HFPO-DA in rodent liver, transcriptomic analyses were conducted on samples from primary mouse, rat and pooled human hepatocytes treated for 12, 24 or 72 hours with various concentrations of HFPO-DA, or established agonists of PPARa (GW7647), PPARg (rosiglitazone), or cytotoxic agents (i.e., acetaminophen or d-galactosamine). Concordance analyses of enriched pathways across chemicals within each species demonstrated greatest concordance between HFPO-DA and PPARa agonist GW7647-treated hepatocytes compared to the other chemicals evaluated. These findings were supported by benchmark concentration modeling and predicted upstream regulator results. In addition, transcriptomic analyses across species demonstrated a greater transcriptomic response in rodent hepatocytes treated with HFPO-DA or agonists of PPARa or PPARg, indicating rodent hepatocytes are more sensitive to HFPO-DA or PPARa/g agonist treatment. These results are consistent with previously published transcriptomic analyses and further support that liver effects in HFPO-DA-exposed rodents are mediated through rodent-specific PPARa signaling mechanisms as part of the MOA for PPARa activator-induced rodent hepatocarcinogenesis.
2024-04-30 | GSE248251 | GEO
Project description:Temporal Concordance between Apical and Transcriptional Points-of-Departure for Chemical Risk Assessment
| PRJNA196610 | ENA
Project description:Expression data of sandwich cultured primary rat hepatocytes incubated to piperazine designer drugs
| PRJNA283856 | ENA
Project description:Transcriptional profiles of rodent hippocampal CA1 tissue during aging and cognitive decline
| PRJNA104011 | ENA