Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular effects of EtOH and Nicotine on normal human oral keratinocytes

ABSTRACT: We have performed gene expression microarry analysis to profile molecular alterations in normal human oral keratinocytes that are induced by EtOH and/or nicotine. Our goal is to examine molecular signatures that are dysregulated by EtOH or nicotine and define the effects of co-use of alcohol and nicotine on normal oral epithelial cells and potentially on carcinogenesis. Primary normal human oral keratinocytes were cultured and treated with various dose of EtOH (0, 20 and 50 mM) and cotreated with various dose of nicotine (0, 0.5 and 1uM) for 24 hours. Total RNA was isolated and subjected to gene expression microarray analysis using Affymetrix Human Genome 2.0 plus.

ORGANISM(S): Homo sapiens

SUBMITTER: Yong Kim

PROVIDER: E-GEOD-57634 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Molecular effects of EtOH and Nicotine on normal human oral keratinocytes

Project description:We have performed gene expression microarry analysis to profile molecular alterations in normal human oral keratinocytes that are induced by EtOH and/or nicotine. Our goal is to examine molecular signatures that are dysregulated by EtOH or nicotine and define the effects of co-use of alcohol and nicotine on normal oral epithelial cells and potentially on carcinogenesis.

2014-05-14 | GSE57634 | GEO

Homo sapiens

Project description:Molecular effects of EtOH and Nicotine on normal human oral keratinocytes

| PRJNA247378 | ENA

Effect of EtOH on transcriptome signatures in human dental pulp stem cells

Project description:We have performed gene expression microarray analysis to profile transcriptomic signatures affected by EtOH in human dental pulp stem cells Established human dental pulp stem cells were treated with different dose of EtOH (0, 1, 5, 10, 20 and 50mM) for a different time periods (24 and 48 hrs). Total RNA was extracted and subjected to gene expression microarray analysis using Affymetrix human genome 2.0 plus array

2014-05-03 | E-GEOD-57255 | biostudies-arrayexpress

Expression data from oral squamous cell carcinoma (OSCC)-derived cell lines and normal oral keratinocytes

Project description:Oral squamous cell carcinoma (OSCC) is a lethal disease and early death usually occurs as a result of local invasion and regional lymph node metastases. We used microarrays to identify down or upregulated genes in OSCCs compared with non-malignant controls. To identify genes whose transcription is deregulated in OSCC, the gene expression profiles of eight OSCC cell lines (H-series and M9) and three primary cultures of normal oral keratinocytes (NKs) were examined using Affymetrix HG-U133A and HG-U133 Plus 2.0 arrays.

2011-09-01 | E-GEOD-31853 | biostudies-arrayexpress

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

Nicotine administration augments abdominal aortic aneurysm progression in rats

Project description:Inflammation and elastin degradation are key hallmarks in the pathogenesis of abdominal aortic aneurysms (AAA). It has been acknowledged that activation of alpha7 nicotinic acetylcholine receptors (α7nAChRs) attenuates inflammation, termed the cholinergic anti-inflammatory pathway (CAP). Thus, we hypothesized that low-dose nicotine, an α7nAChR agonist, impairs the progression of AAAs in rats by activating the CAP. Male Sprague-Dawley rats underwent surgical AAA induction with intraluminal elastase infusion. We compared vehicle rats with rats treated with nicotine (1.25 mg/kg/day) and the aneurysm progression was monitored by weekly ultrasound images for 28 days. Nicotine significantly promoted AAA progression after 28 days of treatment (p=0.031). Additionally, gelatin zymography demonstrated that nicotine significantly reduced pro-matrix metalloprotease (pro-MMP) 2(p=0.029) and MMP9(p=0.030) activity in aneurysmal tissue. No significant difference was found in elastin content or the score of elastin degradation between the groups. Neither infiltrating neutrophils nor macrophages, nor aneurysmal messenger RNA (mRNA) levels of pro- or anti-inflammatory cytokines differed between the vehicle and nicotine group. Finally, no difference in mRNA levels of markers for antioxidative stress or vascular smooth muscle cells contractile phenotype was observed. However, proteomics analyses of non-aneurysmal abdominal aortas revealed that nicotine decreased proteins in the ontology terms inflammation and reactive oxygen species and in contradiction to augmented AAAs. In conclusion, treatment with the given nicotine dose augmented AAA progression in this rat model.

2023-07-20 | PXD040414 | Pride

Effect of EtOH on neural stem cells derived from human embryonic stem cells

Project description:We have performed gene expression microarray analysis to profile transcriptomic signatures affected by EtOH during neural differentiation of human embryonic stem cells H1 human embryonic stem cells were differentiated into neural rosettes and neural progenitor cells in the presence or absence of 20mM EtOH treatment. Undifferentiated passage 40 H1 cells were used as a parental control. Total RNA was isolated from biological duplicates and subjected to gene expression profiling analysis using Affymetrix Human Genome U133 plus 2.0 Array

2014-04-19 | E-GEOD-56906 | biostudies-arrayexpress

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

2008-04-12 | GSE11142 | GEO

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

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

Chronic oral administration of nicotine affects transcriptomic profiling in conditional Presenilin 1/2 knockout mice and wild type mice

Project description:we found that chronic oral (3 months) administration of nicotine had different effects on transcriptomic profiling in prefrontal forebrain cortex of wildtype (WT) and Presenilin 1/2 double knockout mice.

2024-01-01 | GSE211983 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data