Nicotine Modulates the Expression of a Diverse Set of Genes in the Neuronal SH-SY5Y Cell Line

Dunckley, Travis; Lukas, Ronald J.

doi:10.1074/jbc.m210389200

Cited by 73 publications

(75 citation statements)

References 40 publications

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“…Data from higher density genome scanning SNP arrays and assessments of genes for other family members both suggest that human individual differences in other cell adhesion molecule genes could contribute to addiction vulnerability (Q-R Liu, GRU et al, in preparation; HI and GRU, in preparation). Molecules with Ig/fibronectin/single transmembrane domain/tyrosine kinase motifs such as those displayed by NrCAM, molecules with EGF-like motif/single transmembrane domain/tyrosine kinase motifs, and nontransmembrane cell adhesion molecules that contain glycoprotein membrane anchors are each implicated by these studies and/or by studies that document regulation by abused substances (Grigorenko et al, 2002;Miller and Luo, 2002;Dunckley and Lukas, 2003) (HI and GRU, in preparation). Regulatory events that involve NrCAM and other cell adhesion molecules appear to play significant roles in adaptive process that follow drug administration, including those relevant for addiction.…”

Section: Discussionmentioning

confidence: 99%

NrCAM in Addiction Vulnerability: Positional Cloning, Drug-Regulation, Haplotype-Specific Expression, and Altered Drug Reward in Knockout Mice

Ishiguro

Liu

Gong

et al. 2005

Neuropsychopharmacol

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Several lines of evidence support roles for the cell adhesion molecule NrCAM in addictions. Fine mapping within a chromosome 7 region that contains previously linked and associated genomic markers identifies NrCAM haplotypes that are associated with substance abuse vulnerabilities in four samples of abusers and controls. Differential display identifies NrCAM as a drug regulated gene. NrCAM is expressed in neurons linked to reward and memory. NrCAM displays haplotype-specific gene expression in human post-mortem brain samples. Knockout mice display reduced opiate-and stimulant-conditioned place preferences. These observations support NrCAM as a positionally cloned and drug-regulated gene whose variants are likely to change expression and alter substance abuse vulnerabilities in human addictions and animal models of drug reward.

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Section: Discussionmentioning

confidence: 99%

NrCAM in Addiction Vulnerability: Positional Cloning, Drug-Regulation, Haplotype-Specific Expression, and Altered Drug Reward in Knockout Mice

Ishiguro

Liu

Gong

et al. 2005

Neuropsychopharmacol

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“…In addition to influencing neurotransmitter release, a role for nAChRs in the regulation of cell signaling and gene expression has been reported [52] . In neuroblastoma cells, exposure to nicotine influences the expression of a diverse set of genes, including transcription and protein-processing factors, and proteins associated with RNA binding and the plasma membrane [53] . For nAChRs, such transcriptional control is usually triggered by calcium influx directly through the receptors, indirectly through VDCCs, and through release from internal stores [4,[54][55][56][57][58] .…”

Section: Instantaneous Effectsmentioning

confidence: 99%

Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system

2009

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Based on the composition of the five sub units forming functional neuronal nicotinic acetylcholine receptors (nAChRs), they are grouped into either heteromeric (comprising both α and β subunits) or homomeric (comprising only α subunits) receptors. The nAChRs are known to be differentially permeable to calcium ions, with the α7 nAChR subtype having one of the highest permeabilities to calcium. Calcium influx through nAChRs, particularly through the α-bungarotoxin-sensitive α7-containing nAChRs, is a very efficient way to raise cytoplasmic calcium levels. The activation of nAChRs can mediate three types of cytoplasmic calcium signals: (1) direct calcium influx through the nAChRs, (2) indirect calcium influx through voltage-dependent calcium channels (VDCCs) which are activated by the nAChR-mediated depolarization, and (3) calciuminduced calcium release (CICR) (triggered by the first two sources) from the endoplasmic reticulum (ER) through the ryanodine receptors and inositol (1,4,5)-triphosphate receptors (IP 3 Rs). Downstream signaling events mediated by nAChRmediated calcium responses can be grouped into instantaneous effects (such as neurotransmitter release, which can occur in milliseconds after nAChR activation), short-term effects (such as the recovery of nAChR desensitization through cellular signaling cascades), and long-term effects (such as neuroprotection via gene expression). In addition, nAChR activity can be regulated by cytoplasmic calcium levels, suggesting a complex reciprocal relationship. Further advances in imaging techniques, animal models, and more potent and subtype-selective ligands for neuronal nAChRs would help in understanding the neuronal nAChR-mediated calcium signaling, and lead to the development of improved therapeutic treatments.

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“…This criterion was selected after observing that the mean variance of all of the probes was 0.15, and the false positive rate was estimated to be 0.0032%. With similar multiple hybridizations and cDNA microarrays, the fold change of 1.3-1.4 was utilized to identify significant gene expression change in other studies (31)(32)(33). Additionally, significant fold changes required that the 95% CI of the fold change, two standard errors away from the fold change, excluded 1.…”

Section: Methodsmentioning

confidence: 99%

Reduced Expression of the Insulin Receptor in Mouse Insulinoma (MIN6) Cells Reveals Multiple Roles of Insulin Signaling in Gene Expression, Proliferation, Insulin Content, and Secretion

Ohsugi

Cras-Méneur

Zhou

et al. 2005

Journal of Biological Chemistry

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The role of insulin signaling in pancreatic ␤ cells has become increasingly apparent. Stably transformed insulinoma cell lines (MIN6) were created with small interfering RNA resulting in the reduction of insulin receptor (IR) expression up to 80% (insulin receptor knockdown, IRKD⌬80). Functionally perturbed IR signaling was confirmed with the absence of insulin-stimulated insulin receptor substrate 1 tyrosine phosphorylation. Additionally, Akt phosphorylation was reduced and responded poorly to glucose stimulation. Gene expression profiling revealed that reduced IR expression was associated with alterations in expression of >1,500 genes with diverse functions. IRKD cells exhibited low rate of proliferation due to delay in transition from G 0 /G 1 to S phase, whereas susceptibility to apoptosis did not differ from that of control cells. Insulin content was reduced in proportion to the reduction of IR. IRKD cells maintained glucose responsiveness as measured by NAD(P)H generation, whereas Ca 2؉ responses and insulin secretion were enhanced. IRKD⌬80 and control cells were treated with glucose (25 mM) or insulin (100 nM) for 45 min, and gene expression profiles were assessed. Transcriptional activation of several hundred early response genes common to both glucose and insulin stimulation was observed in control cells. In IRKD⌬80 cells, insulin failed to activate any genes as anticipated. Importantly, glucose stimulation of gene expression in IRKD⌬80 cells showed that most genes previously activated by glucose were no longer activated, suggesting a major autocrine/paracrine effect of insulin on glucoseregulated gene expression. On the other hand, there were a number of glucose-regulated genes in the IRKD⌬80 cells that were not previously observed in control cells, suggesting a feedback regulation of insulin signaling on glucose-regulated gene expression. These results demonstrate important roles of the insulin receptor in islet ␤ cell gene expression and function and may serve to elucidate molecular defects in animal models with diminished ␤ cell insulin signaling.Pancreatic ␤ cells dynamically adapt to their environment (1, 2). Changes in plasma glucose concentration along with various hormones and growth factors have been shown to be major determinants of insulin secretion, biosynthesis, and islet mass (3, 4). The islet ␤ cell responds to these changes in its environment by altering its transcriptional responses, and these changes in gene expression ultimately result in altered mass and function. However, the signaling pathways activated by these environmental changes and the ensuing transcriptional events that mediate these biological responses are only beginning to be elucidated. Specifically, the relationships between the signaling pathways activated by glucose and those activated by growth factors such as insulin remain unclear.The roles of insulin as a growth factor in the modulation of ␤ cell mass and function have been implied by the results of recent experiments. Glucose stimulation of ␤ cells in culture ha...

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Nicotine Modulates the Expression of a Diverse Set of Genes in the Neuronal SH-SY5Y Cell Line

Cited by 73 publications

References 40 publications

NrCAM in Addiction Vulnerability: Positional Cloning, Drug-Regulation, Haplotype-Specific Expression, and Altered Drug Reward in Knockout Mice

NrCAM in Addiction Vulnerability: Positional Cloning, Drug-Regulation, Haplotype-Specific Expression, and Altered Drug Reward in Knockout Mice

Nicotinic acetylcholine receptor-mediated calcium signaling in the nervous system

Reduced Expression of the Insulin Receptor in Mouse Insulinoma (MIN6) Cells Reveals Multiple Roles of Insulin Signaling in Gene Expression, Proliferation, Insulin Content, and Secretion

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