GeneSet Information

Tier III GS15464 • Nicotinic dependence genes identified via gene expression in human SH-SY5Y neuroblastoma cells

DESCRIPTION:

Changes in gene expression in neuron-like, SH-SY5Y human neuroblastoma cells, is analyzed following 24 hours of continuous exposure to 1 mM nicotine and several nicotine-induced cellular changes in acetylcholine receptor are found. Microarray analysis of gene expression shows significantly and consistently altered genes during nicotine treatment with a p-value of less than 0.01.

LABEL:

Nicotine Dependence

SCORE TYPE:

P-Value

DATE ADDED:

2009-01-31

DATE UPDATED:

2020-05-06

SPECIES:

AUTHORS:

Konu O, Kane JK, Barrett T, Vawter MP, Chang R, Ma JZ, Donovan DM, Sharp B, Becker KG, Li MD

TITLE:

Region-specific transcriptional response to chronic nicotine in rat brain.

JOURNAL:

Brain research Aug 2001, Vol 909, pp. 194-203

ABSTRACT:

Even though nicotine has been shown to modulate mRNA expression of a variety of genes, a comprehensive high-throughput study of the effects of nicotine on the tissue-specific gene expression profiles has been lacking in the literature. In this study, cDNA microarrays containing 1117 genes and ESTs were used to assess the transcriptional response to chronic nicotine treatment in rat, based on four brain regions, i.e. prefrontal cortex (PFC), nucleus accumbens (NAs), ventral tegmental area (VTA), and amygdala (AMYG). On the basis of a non-parametric resampling method, an index (called jackknifed reliability index, JRI) was proposed, and employed to determine the inherent measurement error across multiple arrays used in this study. Upon removal of the outliers, the mean correlation coefficient between duplicate measurements increased to 0.978+/-0.0035 from 0.941+/-0.045. Results from principal component analysis and pairwise correlations suggested that brain regions studied were highly similar in terms of their absolute expression levels, but exhibited divergent transcriptional responses to chronic nicotine administration. For example, PFC and NAs were significantly more similar to each other (r=0.7; P<10(-14)) than to either VTA or AMYG. Furthermore, we confirmed our microarray results for two representative genes, i.e. the weak inward rectifier K(+) channel (TWIK-1), and phosphate and tensin homolog (PTEN) by using real-time quantitative RT-PCR technique. Finally, a number of genes, involved in MAPK, phosphatidylinositol, and EGFR signaling pathways, were identified and proposed as possible targets in response to nicotine administration. PUBMED: 11478936
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Annotation Information



Brain (D001921)
Gene Expression Regulation (D005786)
Animals (D000818)
Humans (D006801)
Reproducibility of Results (D015203)
Principal Component Analysis (D025341)
Gene Expression Profiling (D020869)
Drug Administration Schedule (D004334)
Microarray Analysis (D046228)
RNA, Messenger (D012333)
Phosphoric Monoester Hydrolases (D010744)
Tumor Suppressor Proteins (D025521)
Therapeutics (D013812)
Literature (D008091)
Potassium Channels, Tandem Pore Domain (D024683)
Potassium Channels (D015221)
Phosphatidylinositols (D010716)
Amygdala (D000679)
Acetylcholine (D000109)
Prefrontal Cortex (D017397)
Rats (D051381)
Tobacco Use Disorder (D014029)
PTEN Phosphohydrolase (D051059)
Nucleus Accumbens (D009714)
Ventral Tegmental Area (D017557)
Oligonucleotide Array Sequence Analysis (D020411)
Cells (D002477)
Transcription, Genetic (D014158)
Organization and Administration (D009934)
Genes, vif (D016341)
DNA, Complementary (D018076)
Neuroblastoma (D009447)
Expressed Sequence Tags (D020224)
Signal Transduction (D015398)
Nicotine (D009538)
Rats, Sprague-Dawley (D017207)
Nicotinic Agonists (D018722)
amygdala (MA:0000887)
brain (MA:0000168)
neuroblastoma (MP:0002039)
nucleus (GO:0005634)
response to nicotine (GO:0035094)
gene expression (GO:0010467)
signaling (GO:0023052)
epidermal growth factor receptor activity (GO:0005006)

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Supported by NIH R01 AA18776 jointly funded by NIAAA and NIDA, and JAX Center for Precision Genetics NIH U54 OD 020351