GeneSet Information

Tier III GS18839 • Downregulated Nicotine-dependent genes in human neuroblastoma (SH-SY5Y) cells

DESCRIPTION:

Human neuroblastoma (SH-SY5Y) cells were chronically exposed to nicotine to discover if gene expression was responsible for the long term effects of nicotine on the nervous system and for the up-regulation of acetylcholine receptors upon nicotine exposure. Seventeen genes were found to be differentially expressed. Of these, the genes reported here were down-regulated.

LABEL:

Hum. DnReg Nic. Depend.

SCORE TYPE:

Binary

DATE ADDED:

2009-03-20

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

Dunckley T, Lukas RJ

TITLE:

Nicotine modulates the expression of a diverse set of genes in the neuronal SH-SY5Y cell line.

JOURNAL:

The Journal of biological chemistry May 2003, Vol 278, pp. 15633-40

ABSTRACT:

Nicotine exposure can have long lasting effects on nervous system function, some of which must contribute to nicotine dependence. Up-regulation, an increase in numbers of radioligand-binding nicotinic acetylcholine receptors (nAChR), occurs on exposure to nicotine at high concentrations. To determine whether altered gene expression might account for long term changes and up-regulation following nicotine exposure, we assessed effects of 1 h of 1 mm nicotine exposure on alteration of gene expression in the neuron-like SH-SY5Y neuroblastoma clonal line. Repeat and cross-controlled microarray analyses yielded a list of 17 genes from the initially screened approximately 5,000 whose expression was consistently altered following nicotine treatment. Subsequent quantitative, real time reverse transcriptase PCR analyses confirmed altered expression in 14 of 16 genes tested. Further, the general nAChR antagonist, d-tubocurarine, blocked all but two of the observed changes in gene expression, indicating that these changes are dependent on nAChR activation. Use of other antagonists revealed that nAChR subtypes can differentially affect gene expression. The genes affected code for proteins that may be broadly categorized into four groups: transcription factors, protein processing factors, RNA-binding proteins, and plasma membrane-associated proteins. Our results suggest that nicotinic activation of nAChR may have a broad role in affecting cellular physiology through modulating gene expression. PUBMED: 12588870
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Annotation Information

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Gene Expression Regulation (D005786)
Cell Line (D002460)
Tubocurarine (D014403)
Tumor Cells, Cultured (D014407)
Cell Adhesion Molecules, Neuronal (D015816)
Humans (D006801)
Receptors, Nicotinic (D011978)
Polymerase Chain Reaction (D016133)
Physiology (D010827)
RNA, Messenger (D012333)
Attention (D001288)
Proteins (D011506)
Therapeutics (D013812)
Role (D012380)
Time (D013995)
Reverse Transcriptase Polymerase Chain Reaction (D020133)
Acetylcholine (D000109)
Nervous System (D009420)
Tobacco Use Disorder (D014029)
Up-Regulation (D015854)
RNA-Directed DNA Polymerase (D012194)
Oligonucleotide Array Sequence Analysis (D020411)
Plasma (D010949)
Cells (D002477)
RNA-Binding Proteins (D016601)
Transcription Factors (D014157)
Membrane Proteins (D008565)
Affect (D000339)
DNA-Directed RNA Polymerases (D012321)
Vimentin (D014746)
Neuroblastoma (D009447)
Set (Psychology) (D012718)
Receptors, Cholinergic (D011950)
Nicotine (D009538)
plasma (MA:0002501)
nervous system (MA:0000016)
nervous (MP:0008912)
neuroblastoma (MP:0002039)
cell (GO:0005623)
protein processing (GO:0016485)
gene expression (GO:0010467)

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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