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An epigenetic mechanism mediates developmental nicotine effects on neuronal structure and behavior

ABSTRACT: An epigenetic mechanism mediates developmental nicotine effects on neuronal structure and behavior

PROVIDER: PRJNA319981 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3466220.fastq.gz	Fastqsanger.gz
	SRR3466230.fastq.gz	Fastqsanger.gz
	SRR3466221.fastq.gz	Fastqsanger.gz
	SRR3466231.fastq.gz	Fastqsanger.gz
	SRR3466222.fastq.gz	Fastqsanger.gz

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Developmental nicotine mediated gene expression and epigenetic change effects on neuronal structure and behavior [ChIP-seq]

Project description:Developmental nicotine exposure causes persistent changes in cortical neuron morphology and in behavior. We used microarray screening to identify master transcriptional or epigenetic regulators mediating these effects of nicotine and discovered increases in Ash2l, a component of a histone methyltransferase complex. We therefore examined genome-wide changes in H3MeK4 tri-methylation, a mark induced by the Ash2l complex associated with increased gene transcription. A significant number of regulated promoter sites were involved in synapse maintenance. We found that Mef2c interacts with Ash2l and mediates changes in H3MeK4 trimethylation. Knockdown of Ash2l or Mef2c abolishes nicotine-mediated alterations of dendritic complexity in vitro and in vivo, and attenuates nicotine-dependent changes in passive avoidance behavior. In contrast, overexpression mimics nicotine-mediated alterations of neuronal structure and passive avoidance behavior. These studies identify Ash2l as a novel target induced by nicotinic stimulation that couples developmental nicotine exposure to changes in brain epigenetic marks, neuronal structure and behavior. Cortical Histone 3 Lysine 4 tri-methylation profiles of 3 month old C57BL6/J mice were generated by deep sequencing, in triplicate or quadruplicate, using Illumina GAII

2016-05-30 | E-GEOD-80788 | biostudies-arrayexpress

Developmental nicotine mediated gene expression and epigenetic change effects on neuronal structure and behavior [ChIP-seq]

2016-05-30 | GSE80788 | GEO

Developmental nicotine mediated gene expression and epigenetic change effects on neuronal structure and behavior [gene expression]

2016-05-30 | E-GEOD-80787 | biostudies-arrayexpress

Developmental nicotine mediated gene expression and epigenetic change effects on neuronal structure and behavior [gene expression]

2016-05-30 | GSE80787 | GEO

An epigenetic mechanism mediates developmental nicotine effects on neuronal structure and behavior

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-30 | E-GEOD-80789 | biostudies-arrayexpress

An epigenetic mechanism mediates developmental nicotine effects on neuronal structure and behavior

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-05-30 | GSE80789 | GEO

An epigenetic mechanism mediates developmental nicotine effects on neuronal structure and behavior.

Project description:Developmental nicotine exposure causes persistent changes in cortical neuron morphology and in behavior. We used microarray screening to identify master transcriptional or epigenetic regulators mediating these effects of nicotine and discovered increases in Ash2l mRNA, encoding a component of a histone methyltransferase complex. We therefore examined genome-wide changes in trimethylation of histone H3 on Lys4 (H3K4me3), a mark induced by the Ash2l complex associated with increased gene transcription. A large proportion of regulated promoter sites were involved in synapse maintenance. We found that Mef2c interacts with Ash2l and mediates changes in H3K4me3. Knockdown of Ash2l or Mef2c abolished nicotine-mediated alterations of dendritic complexity in vitro and in vivo, and attenuated nicotine-dependent changes in passive avoidance behavior. In contrast, overexpression mimicked nicotine-mediated alterations of neuronal structure and passive avoidance behavior. These studies identify Ash2l as a target induced by nicotinic stimulation that couples developmental nicotine exposure to changes in brain epigenetic marks, neuronal structure and behavior.

| S-EPMC4925298 | biostudies-literature

Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

Project description:Purpose: The goal of this study is to compare the effects of inhaled nicotine on aortic gene expression and the role of the alpha7 nicotinic acetylcholine receptor (alpha7-nAChR) in mediating the nicotine effects. Methods: WT and alpha7-nAChR knockout (KO) mice at 5-month of age were exposed to nicotine vapor or room air for a total of 12 weeks. Total RNA was extracted from thoracic aortas using RNeasy Plus mini kit followed by library preparation using SMART-Seq v4 Ultra Low Input RNA Kit. Illumina next generation sequencing was performed using the NextSeq 500 system with the high output flow cell (up to 800 M paired end reads). Results: A total of 179 differentially expressed genes (149 upregulated and 30 downregulated, adjusted P-value < 0.1) were found in thoracic aortas from WT mice exposed to nicotine vapor compared to those exposed to room air. In contrast, only 7 non-overlapping genes were found to be differentially expressed in alpha7-nAChR KO mice exposed to nicotine compared to the air controls. Conclusions: Our study suggests that nicotine-induced changes in vascular gene expression is largely mediated by the alpha7-nAChR.

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

Project description: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.

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Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

Project description:Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

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