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

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

PROVIDER: PRJNA803731 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17893167_1.fastq.gz	Fastqsanger.gz
	SRR17893167_2.fastq.gz	Fastqsanger.gz
	SRR17893168_1.fastq.gz	Fastqsanger.gz
	SRR17893168_2.fastq.gz	Fastqsanger.gz
	SRR17893169_1.fastq.gz	Fastqsanger.gz

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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.

2022-02-08 | GSE196184 | GEO

whole brains from nicotinic acetylcholine receptor subunit mutant mice and littermate controls

Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Keywords: knockout mice, nicotinic acetylcholine receptor

2006-09-22 | GSE5320 | GEO

Short-term depletion of nicotinic acetylcholine receptor subunits in Drosophila enterocytes

Project description:Bulk RNAseq from whole Drosophila melanogaster guts expressing either mCherry-RNAi (control) or RNAi against nicotinic acetylcholine receptor subunits β1 and β3 (nAchRβ1 and nAchRβ3) under control of a enterocyte-specific driver to assess their role in barrier function.

2023-08-23 | GSE236069 | GEO

Chronic nicotine exposure (kuo-affy-human-232930)

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. Keywords: time-course

2008-04-19 | GSE11208 | GEO

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

2008-06-11 | E-GEOD-11208 | biostudies-arrayexpress

RNA sequencing data describing transcriptional changes in aorta of ApoE-/- mice after alpha 7 nicotinic acetylcholine receptor (α7nAChR) stimulation.

Project description:This manuscript is a companion paper to Ulleryd M.U. et al (1). Data shown here include RNA sequencing data from whole aorta of ApoE-/- mice treated with the alpha 7 nicotinic acetylcholine receptor (α7nAChR) agonist AZ6983 for 8 weeks using subcutaneously implanted osmotic minipumps. 1. Ulleryd MA, Mjornstedt F, Panagaki D, Yang LJ, Engevall K, Gutierrez S, et al. Stimulation of alpha 7 nicotinic acetylcholine receptor (α7nAChR) inhibits atherosclerosis via immunomodulatory effects on myeloid cells Re-submitted. 2019.

2019-10-29 | GSE131162 | GEO

Transcription profiling of brains from wild type and beta4 nicotinic acetylcholine receptor (nAChR) subunit deficient mice to identify genes that might be related to beta4-containing nAChRs activity

Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Experiment Overall Design: The experimental groups included six wild-type mice and five beta4-/- mice. All mice were 6-9 weeks old. Total RNA was extracted from whole brain tissue of the mice.

2007-11-27 | E-GEOD-5320 | biostudies-arrayexpress

α7 nicotinic acetylcholine receptor signaling modulates the inflammatory phenotype of fetal brain microglia: first evidence of interference by iron homeostasis.

Project description:We sequenced mRNA from 7 microglia extracted from sheep fetuses exposed to LPS, agonist and antagonist of α7 nicotinic acetylcholine receptor to determine signaling pathway through modeling of α7 during inflammation.

2017-08-11 | GSE101857 | GEO

Nicotine effect on CEM model T cell line (kuo-affy-human-232861)

Project description:The long-term objective of this project is to establish roles played in development and function of the immune system by nicotinic acetylcholine receptors (nAChR) and exposure to the tobacco alkaloid, nicotine. The planned gene chip studies will allow us to assess effects of nicotine exposure on gene expression in a model T cell line, and the findings are expected to help direct further efforts. One of the biomedically-relevant hypotheses of this project is that tobacco use and nicotine exposure affect immune system development. To establish effects of nicotine exposure on gene expression in the CEM model T cell line. Immune system nAChR acting as ion channels or via novel signaling cascades mediate their effects on T cell development by altering expression of genes involved in T cell receptor rearrangements, cytokine expression, and cell death/survival decisions. CEM cells will be treated for one hour or one day with an effective dose of nicotine or with the same medium change but in the absence of nicotine. Keywords: nicotine, T cell line

2008-04-11 | E-GEOD-11142 | biostudies-arrayexpress

Habenular Tcf7l2 links nicotine addiction to diabetes

Project description:Nicotine contained in tobacco smoke increases blood glucose levels in humans, and the risk of developing diabetes is dramatically increased in habitual smokers. Little is currently known about how nicotine increases blood glucose levels or the relevance of this action to either the persistence of the smoking habit or the pathophysiology of diabetes in smokers. Here, we show that the diabetes-associated gene Tcf7l2 is highly expressed in the medial habenula (mHb), where it regulates the function of local nicotinic acetylcholine receptors. We find that Tcf7l2 mutant (Tcf7l2mut) rats consume far greater quantities of nicotine than wild-type rats. Similarly, CRISPR-mediated cleavage of wild-type Tcf7l2 in the mHb increases nicotine intake in mice. Polysynaptic tracing identified a connection from the mHb to the pancreas, and nicotine-induced activation of the mHb elevates blood glucose. This effect is mimicked by chemogenetic stimulation of the mHb and blocked by Tcf7l2 knockdown in mHb. A history of nicotine consumption elevates circulating levels of the pancreas-derived hormones glucagon and insulin and precipitates diabetes-like dysregulation of blood glucose homeostasis in wild-type rats, whereas Tcf7l2mut rats are resistant to these actions of nicotine. Our findings suggest that Tcf7l2 regulates the stimulatory actions of nicotine on the habenula-pancreas axis, linkings the addictive properties of nicotine to its diabetes-promoting actions.

2019-09-10 | GSE137118 | GEO

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