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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of rat cerebellum and hippocampus following exposure to neurotoxicant Aroclor 1254

ABSTRACT: Pregnant rats (Long-Evans) were dosed perinatally with 0 or 6Â mg/kg/day of Aroclor 1254 from gestation day 6 through postnatal day (PND) 21. Gene expression in cerebellum and hippocampus from PND7 and PND14 animals was analyzed with an emphasis on developmental aspects. Changes in gene expression (>= 1.5 fold) in control animals identified normal developmental changes. These basal levels of expression were compared to data from Aroclor 1254-treated animals to determine the impact of gestational PCB exposure on developmental parameters. The results indicate that the expression of a number of developmental genes related to cell cycle, synaptic function, cell maintenance, and neurogenesis is significantly altered from PND7 to PND14. Aroclor 1254 treatment appears to dampen the overall growth-related gene expression levels in both regions with the effect being more pronounced in the cerebellum. Functional analysis suggests that Aroclor 1254 delays maturation of the developing nervous system, with the consequences dependent on the ontological state of the brain area and the functional role of the individual gene. Experiment Overall Design: Pregnant rats (Long-Evans) were dosed perinatally with 0 or 6Â mg/kg/day of Aroclor 1254 from gestation day 6 through postnatal day (PND) 21. Gene expression in cerebellum and hippocampus from PND7 and PND14 animals was analyzed with an emphasis on developmental aspects.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Jennifer Fostel

PROVIDER: E-GEOD-13793 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiles in the cerebellum and hippocampus following exposure to neurotoxicant Aroclor 1254

Project description:Pregnant rats (Long-Evans) were dosed perinatally with 0 or 6 mg/kg/day of Aroclor 1254 from gestation day 6 through postnatal day (PND) 21. Gene expression in cerebellum and hippocampus from PND7 and PND14 animals was analyzed with an emphasis on developmental aspects. Changes in gene expression (≥ 1.5 fold) in control animals identified normal developmental changes. These basal levels of expression were compared to data from Aroclor 1254-treated animals to determine the impact of gestational PCB exposure on developmental parameters. The results indicate that the expression of a number of developmental genes related to cell cycle, synaptic function, cell maintenance, and neurogenesis is significantly altered from PND7 to PND14. Aroclor 1254 treatment appears to dampen the overall growth-related gene expression levels in both regions with the effect being more pronounced in the cerebellum. Functional analysis suggests that Aroclor 1254 delays maturation of the developing nervous system, with the consequences dependent on the ontological state of the brain area and the functional role of the individual gene. Keywords: time course, stress response

2009-01-31 | GSE13793 | GEO

Toxicogenomic Analysis of Gender, Chemical, and Dose Effects in Livers of TCDD- or Aroclor 1254-Exposed Rats

Project description:Chronic exposure of Sprague-Dawley (SD) rats to either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or Aroclor 1254 results in female-selective induction of hepatic tumors. The relative potency of dioxins and PCB mixtures, such as Aroclor 1254, is often estimated using the internationally endorsed toxic equivalency (TEQ) approach. Comparing the genome wide changes in gene expression in both genders following exposure to toxic equivalent doses of these chemicals should identify critical sets of early response genes while further defining the concept of the TEQ of halogenated aromatic hydrocarbons. Aroclor 1254 at 0.6, 6.0 and 60 mg/kg body weight and TEQ doses of TCDD (0.3 and 3.0 µg/kg), calculated to match the top two Aroclor 1254 doses, were orally administered to SD rats for three consecutive days. Day 4 gene expression in hepatic tissue was determined using microarrays. A linear mixed-effects statistical model was developed to analyze the data in relation to treatment, gender, and gender*treatment (G*T) interactions. The genes most changed included 54 genes with and 51 genes without a significant model G*T term. The known aryl hydrocarbon receptor (AHR) battery genes (Cyp1a1, Cyp1a2, Cyp1b1, Aldh3a1), and novel genes, responded in a TEQ dose-dependent manner in both genders. However, an important observation was the apparent disruption of sexually dimorphic basal gene expression, particularly for female rats. Since many of these genes are involved in steroid metabolism, exposure to either TCDD or Aroclor 1254 could disrupt proliferative signals more in female rats as a possible consequence of altered estrogen metabolism. This study extends the findings of previous rodent bioassays by identifying groups of genes, other than the well-characterized AHR response genes, whose disruption may be important in the tumorigenic mechanism in this rat strain. Keywords: dose response, Multifactor Linear Model

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Project description:Gene expression profiles in the cerebellum and hippocampus following exposure to neurotoxicant Aroclor 1254

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Glycation modulates glutamatergic signaling and exacerbates ParkinsonÃ¢â‚¬â„¢s disease-like phenotypes

Project description:Alpha-synuclein (aSyn) is a central player in the pathogenesis of synucleinopathies due to its accumulation in typical protein aggregates in the brain. However, it is still unclear how it contributes to neurodegeneration. Type-2 diabetes mellitus is a risk factor for ParkinsonÃ¢â‚¬â„¢s disease (PD) and, interestingly, a common molecular alteration among these disorders is the age-associated increase in protein glycation. We hypothesized that glycation-induced neuronal dysfunction might be a contributing factor in synucleinopathies. Here, we dissected the specific impact of methylglyoxal (MGO, a glycating agent) in mice overexpressing aSyn in the brain. We found that MGO-glycation potentiates motor, cognitive, olfactory, and colonic dysfunction in aSyn transgenic (Thy1-aSyn) mice that received a single dose of MGO via intracerebroventricular (ICV) injection. aSyn accumulates in the midbrain, striatum, and prefrontal cortex, and protein glycation is increased in the cerebellum and midbrain. SWATH mass spectrometry analysis, used to quantify changes in the brain proteome, revealed that MGO mainly increase glutamatergic-associated proteins in the midbrain (NMDA, AMPA, glutaminase, VGLUT and EAAT1), but not in the prefrontal cortex, where it mainly affects the electron transport chain. Notably, the glycated proteins in the midbrain of Thy1-aSyn mice that received MGO strongly correlate with PD and dopaminergic pathways. Overall, we demonstrated that MGO-induced glycation accelerates PD-like sensorimotor and cognitive alterations and suggest that the increase of glutamatergic signaling may underly these events. Our study sheds new light into the enhanced vulnerability of the midbrain in PD-related synaptic dysfunction and suggests that glycation suppressors and anti-glutamatergic drugs may hold promise as disease-modifying therapies for synucleinopathies.

2022-05-20 | PXD032832 | Pride

E-GEOD-13793

Project description:Transcription profiling of rat cerebellum and hippocampus following exposure to neurotoxicant Aroclor 1254

2015-08-28 | E-GEOD-13793 | ExpressionAtlas

Signature of human hepatocytes treated with Aroclor1254

Project description:In order to determine molecular rules for transcriptional regulation of targeted genes to explain in part the pleiotropic effect observed in animals and humans upon exposure to Aroclor 1254 we treated human hepatocytes with Aroclor1254 and analysed RNA expression using a Nimblegene human custom array. Keywords: Human hepatocytes, Aroclor1254 treatment, 20µM, 72h

2006-08-01 | GSE5213 | GEO

Transcription profiling of liver from immature Platichthys flesus treated with model toxicants

Project description:Using the GENIPOL flounder cDNA microarray, we assessed the temporal transcriptomic responses of Platichthys flesus to model toxicants over a 16 day timespan. Immature fish were treated by intraperitoneal injection with cadmium chloride (50 micrograms/kg in saline), 3-methylcholanthrene (25mg/kg in olive oil), Aroclor 1254 (50mg/kg in olive oil), tert-butyl-hydroperoxide (5mg/kg in saline), lindane (25 mg/kg in olive oil), perfluoro-octanoic acid (100mg/kg in olive oil), olive oil or saline (0.9%). Hepatic gene expression changes were determined 1,2,4,8 and 16 days post-injection in comparison with time-matched carrier controls.

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Project description:Plaques consisting of amyloid-ÃŽÂ² (AÃŽÂ²) in the brain are characteristic for patients with AlzheimerÃ‚Â´s disease. AÃŽÂ² is enzymatically generated of the amyloid precursor protein. Furthermore, neprilysin, an AÃŽÂ²-degrading enzyme, and its main activator the neuropeptide somatostatin (SST) are downregulated in AlzheimerÃ‚Â´s disease. In the fusion protein SST-scFv8D3, SST is recombinantly fused to a blood-brain barrier transporter. The aim of this study was to study the effect of SST-scFv8D3 on the proteome of different brain regions in order to elucidate the anti-AlzheimerÃ‚Â´s disease effects of this construct. SST-scFv8D3 and phosphate buffered saline (PBS) respectively were injected into transgenic mice of an AlzheimerÃ‚Â´s disease model with the Swedish mutation (AÃŽÂ²PP KM670/671NL) every 36 hours (three times in total). Homogenates of the hippocampus, the cerebellum and the rest of the cerebrum were lysed. Afterwards, filter aided tryptic digestion was performed. The resulting peptides were analyzed using LC-UDMSE. The data was searched against a randomized mouse database and label-free quantification analysis was done. In total 1869 proteins were found. Only the proteome of the hippocampus was affected by the treatment with SST-scFv8D3. 55 proteins were significantly up and 105 down regulated compared to the PBS treated mice. Among these were mitochondrial and synaptic proteins as well as some involved in neuronÃ‚Â´s development indicating anti-Alzheimer disease effects of SST-scFv8D3 and supporting the future use of SST-scFv8D3 as a treatment option.

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Project description:Prenatal iron deficiency (pID) has been described to increase the risk for neurodevelopmental disorders such as autism and schizophrenia; however, the precise molecular mechanisms are still unknown. Here, we utilized high throughput mass spectrometry to examine the proteomic effects of pID in adulthood on the rat frontal cortex area (FCA). In addition, the FCA proteome was examined in adulthood following risperidone treatment in adolescence to see if these effects could be prevented. We identified 1501 proteins of which 100 were significantly differentially expressed in the FCA at post-natal day 90. Pathway Analysis of proteins affected by pID revealed changes in metabolic processes, including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Akt signaling. Interestingly, most of these protein changes were not present in the adult pID offspring who received risperidone in adolescence. Behavioral testing of pID rats demonstrated social impairment and poor performance during novelty-induced exploration in pID animals in line with a abnormal neurodevelopmental phenotype. Considering the link between prenatal iron deficiency and several neurodevelopmental disorders such as autism and schizophrenia these presented results bring new perspectives to understand the role of iron in metabolic pathways and provide novel biomarkers for future studies of prenatal iron deficiency.

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