Effects of a pyrethroid pesticide deltamethrin on gene expression profiles in mouse neuroblastoma Neuro2a cell
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PROVIDER: PRJNA734568 | ENA |
REPOSITORIES: ENA
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Project description:Pyrethroids are one of the most commonly used classes of synthetic pesticides detected from all individuals in every part of the world; however, the mechanisms underlying the neurotoxicity of pyrethroids were still remain unclear. To understand neurotoxic mechanisms of DM, we investigated transcriptome changes by exposure to a pyrethroid pesticide deltamethrin (DM) in the mouse neuroblastoma Neuro2a cell.
2021-06-03 | GSE176000 | GEO
Project description:Neurodevelopmental disorders (NDD) are a category of pervasive disorders of the developing nervous system with few or no recognized biomarkers. A significant portion of the risk for NDD, including ADHD, is contributed by the environment, and exposure to pyrethroid pesticides during pregnancy has been identified as a potential risk factor for NDD in the unborn child. We recently showed that low-dose developmental exposure to the pyrethroid pesticide deltamethrin (DPE) in mice causes male-biased changes to ADHD- and NDD-relevant behaviors as well as the striatal dopamine system. Here, we used a multiomics approach to determine the broadest possible set of pharmacologically relevant changes in mouse brain resulting from DPE. Using a litter-based, split-sample design, we deltamethrin mouse dams during pregnancy and lactation to deltamethrin (3 mg/kg or vehicle every 3 days) at a concentration well below the EPA-determined benchmark dose used for regulatory guidance. The male offspring were raised to adulthood, euthanized, and whole brain samples pulverized and divided for split-sample transcriptomics, kinomics and multiomics integration. The transcriptome revealed alterations to multiple canonical clock genes. The kinome revealed changes in the activity of multiple kinases involved in synaptic plasticity, and broadly in the AGC kinase family. Multiomics integration revealed a dysregulated protein-protein interaction network containing primary clusters for MAP kinase cascade, synaptic function, and regulation of apoptosis. These results demonstrate that DPE causes a multi-modal biophenotype in the brain relevant to ADHD and identifies new potential avenues for therapeutics.
2023-08-28 | GSE241185 | GEO
Project description:To investigate a role of mKIAA genes in early stage of neurite outgrowth, in vitro time course experiment was performed using the mouse neuroblastoma Neuro2A cells and all-trans-retinoic acid. Six time points of 8 biological replicates were performed.These data were normalized by median intensities and subtracted background intensities. NOTE: Outlier involved several data were not deposited. Keywords: time-course
2005-04-28 | GSE2570 | GEO
Project description:Ascertain the transcriptional response of the major malaria vector Anopheles coluzzii to the pyrethroid deltamethrin over ten time points.
2021-01-01 | E-MTAB-9422 | biostudies-arrayexpress
Project description:Pyrethroids are neurotoxicants that disrupt nervous system function by interacting with a variety of membrane bound ion channels on neuronal plasma membranes. This study is designed to investigate the transcriptional events downstream of pyrethroid-induced disruption of nervous system excitability. Adult, male Long-Evans rats were orally dosed in vivo with a single dose of either permethrin (1, 10, or 100 mg/kg) or deltamethrin (0.3, 1, 3 mg/kg) at levels that produce only modest behaviroal effects in the whole animal (Wolansky et al. 2006). Transcriptional profiles were obtained from frontal cerebrocortical tissue 6 hours after acute exposure. The primary goals were 1) to identify dose-responsive biomarkers of effect for pyrethroids and 2) identify sensitive intracellular signaling or metabolic pathways sensitive to pyrethroid compounds. Keywords: dose response
2007-10-15 | GSE7955 | GEO
Project description:Custom microarrays were used to examine differential gene expression between pyrethroid resistant vs pyrethroid susceptible phenotypes of the dengue vector mosquito Aedes aegypti. Pyrethroid resistant population were from Cayenne (French Guiana, GUY), Baie Mahault (Guadeloupe, GUA) and Noumea (New Caledonia, CAL) whilst New Orleans lab colony represented the lab susceptible strain Pools of total RNA was extracted from the whole bodies of 3 day old female mosquitoes that had survived exposure to 0.06% deltamethrin (for GUY, GUA, CAL) . Single colour hybridization experiments were performed using labelled cDNA on the Agilent 'Aedes aegypti detox chip plus': A-MTAB-574. Four unique biological replicates per population were used in the study
2015-11-08 | E-MTAB-4022 | biostudies-arrayexpress
Project description:Pyrethroids are neurotoxicants that disrupt nervous system function by interacting with a variety of membrane bound ion channels on neuronal plasma membranes. This study is designed to investigate the transcriptional events downstream of pyrethroid-induced disruption of nervous system excitability. Adult, male Long-Evans rats were orally dosed in vivo with a single dose of either permethrin (1, 10, or 100 mg/kg) or deltamethrin (0.3, 1, 3 mg/kg) at levels that produce only modest behaviroal effects in the whole animal (Wolansky et al. 2006). Transcriptional profiles were obtained from frontal cerebrocortical tissue 6 hours after acute exposure. The primary goals were 1) to identify dose-responsive biomarkers of effect for pyrethroids and 2) identify sensitive intracellular signaling or metabolic pathways sensitive to pyrethroid compounds. Experiment Overall Design: In total 60 samples were analyzed in the present study: vehicle control (n = 12), 1 mg/kg permethrin (n=8), 10 mg/kg permethrin (n = 8), 100 mg/kg permethrin (n = 8), 0.3 mg/kg deltamethrin (n = 8), 1 mg/kg deltamethrin (n = 8), 3 mg/kg deltamethrin (n = 8). Transcriptional profiles for each test subject were obtained independently, without sample pooling. Experiment Overall Design: The publication will include an Appendix Table comparing the variability of RMA values (see Sample VALUE columns) to that of GCOS values (see Sample .CHP files).
2008-06-17 | E-GEOD-7955 | biostudies-arrayexpress
Project description:Organophosphate and pyrethroid pesticides are among the most extensively used insecticides worldwide. Prenatal exposures to both classes of pesticides have been linked to a wide range of neurobehavioral deficits in the offspring. The placenta is a neuroendocrine organ and the crucial regulator of the intrauterine environment; early-life toxicant exposures could impact neurobehavior by disrupting placental processes. Female C57BL/6J mice were exposed via oral gavage to an organophosphate, chlorpyrifos (CPF) at 5 mg/kg, a pyrethroid, deltamethrin (DM), at 3 mg/kg, or vehicle only control (CTL). Exposure began two weeks before breeding and continued every three days until euthanasia at gestational day 17. The transcriptomes of fetal brain (CTL n=18, CPF n= 6, DM n=8) and placenta (CTL n=19, CPF n= 16, DM n=12) were obtained through RNA sequencing, and resulting data was evaluated using weighted gene co-expression networks, differential expression, and pathway analyses. Fourteen brain gene co-expression modules were identified; CPF exposure disrupted the module related to ribosome and oxidative phosphorylation, whereas DM disrupted the modules related to extracellular matrix and calcium signaling. In the placenta, network analyses revealed 12 gene co-expression modules. While CPF exposure disrupted modules related to endocytosis, Notch and Mapk signaling, DM exposure dysregulated modules linked to spliceosome, lysosome and Mapk signaling pathways. Overall, in both tissues, CPF exposure impacted oxidative phosphorylation, while DM was linked to genes involved in spliceosome and cell cycle. The transcription factor Max involved in cell proliferation was overexpressed by both pesticides in both tissues. In summary, gestational exposure to two different classes of pesticide can induce similar pathway-level transcriptome changes in the placenta and the brain; further studies should investigate if these changes are linked to neurobehavioral impairments.
2023-04-06 | GSE228777 | GEO
Project description:Ribosome profiling (Ribo-Seq) and RNA-Seq analysis of mouse neuroblastoma (Neuro2a) cells infected with Japanese Encephalitis Virus (JEV) P20778 Vellore strain. At 18 h post infection (p.i.), infected cells were treated with either cycloheximide (translation elongation inhibitor) or in combination with harringtonine (translation initiation inhibitor). Ribo-Seq libraries were prepared using a broad range of fragment lengths (25 to 70 nucleotides) and deep sequenced. This allowed for estimation of ribosomal frameshifting efficiency and discovery of a novel upstream open reading frame (uORF) in JEV along with perturbations in ribosome-associated tRNA levels upon JEV infection.
2021-07-05 | E-MTAB-9352 | biostudies-arrayexpress
Project description:Neonicotinoids are one of most widely used pesticides targeting nicotinic acetylcholine receptors (nAChRs) of insects and suspected to have adverse effects on mammals by laboratory testing on rodents. Recent epidemiological evidence revealed the increasing amounts of neonicotinoids detected from human samples, rising a critical question whether neonicotinoids affect to human health. We investigated potential effects of a neonicotinoid pesticide, clothianidin (CTD) on human neuroblastoma SH-SY5Y cells as a model of nervous systems of human. Transcriptional analyses using GeneChip system were also performed to understand the effects of CTD on global gene expression.
2019-02-06 | GSE126103 | GEO