Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human model neuronal cell lines after chronic nicotine exposure

ABSTRACT: The long-term goal of this project is to establish whether and how chronic nicotine exposure affects nervous system function. The biological targets of nicotine action are diverse members of the superfamily of neurotransmitter-gated ion channels called nicotinic acetylcholine receptors (nAChR). nAChR play multiple, critical roles in chemical signaling throughout the brain and body. They also must be involved in nicotine dependence, which drives tobacco product use responsible for tremendous economic and personal costs. To define changes in gene expression induced by nicotine exposure in a model neuronal cell lines expressing at least two nicotinic receptor subtypes. Nicotine exposure exerst at least some of its effects on nervous system function by altering gene expression. Cells of the SH-SY5Y human neuroblastoma will be exposed to an efficacious dose of nicotine or to control medium for two different periods.

ORGANISM(S): Homo sapiens

SUBMITTER: Elizabeth Salomon

PROVIDER: E-GEOD-11208 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Nicotine, acting through the neuronal nicotinic acetylcholine receptors (nAChR), can induce seizures in mice. We aimed to study brain transcriptional response to seizure and to identify genes whose expression is altered after nicotine-induced seizures. Whole brains of untreated mice were compared to brains one hour after seizure activity, using Affymetrix U74Av2 microaarays. Experimental groups included wild-type mice and both nicotine-induced seizures sensitive and resistant nAChR mutant mice. Each genotype group received different nicotine doses to generate seizures. This approach allowed the identification of significantly changed genes whose expression was dependent on seizure activity, nicotine administration or both, but not on the type of nAChR subunit mutation or the amount of nicotine injected. Significant expression changes were detected in 62 genes (p < 0.05, FDR correction). Among them, GO functional annotation analysis determined that the most significantly over-represented categories were of genes encoding MAP kinase phosphatases, regulators of transcription and nucleosome assembly proteins. In-silico bioinformatic analysis of the promoter regions of the 62 changed genes detected the significant enrichments of 16 transcription regulatory elements (TREs), creating a network of transcriptional regulatory responses to seizures. The TREs for ATF and SRF were most significantly enriched, supporting their association with seizure activity. Our data suggest that nicotine-induced seizure in mice is a useful model to study seizure activity and its global brain transcriptional response. The differentially expressed genes detected here can help understand the molecular mechanisms underlying seizures in animal models, and may also serve as candidate genes to study epilepsy in humans. Experiment Overall Design: Whole brain expression profiles were determined in two experimental groups of mice, sixteen mice that were not treated with nicotine and twelve mice one hour after experiencing nicotine-induced seizure. The untreated group included six wild-type mice, five alpha7+/T and five beta4-/- mice. The group of mice that underwent nicotine-induced seizures included three wild-types, five alpha7+/T and four beta4-/- mice. Different doses of nicotine were injected intraperitoneally (i.p.) to each genotype group of mice in order to achieve a similar seizure score in all three genotypes.

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Transcription profiling of human model neuronal cell lines after chronic nicotine exposure

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