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Series GSE5056 Query DataSets for GSE5056
Status Public on Nov 21, 2006
Title Airway epithelium, large airways, phenotypically normal smokers vs non-smokers, MAS5 (HuGeneFL)
Organism Homo sapiens
Experiment type Expression profiling by array
Summary Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers
The microarray data deposited here is from 44 HuGeneFL GeneChips, from 9 normal non-smokers and 13 phenotypic normal smokers, large airways, 2 samples per individual, one from the right lung and one from the left lung. These samples were previously described in Hackett NR, Heguy A, Harvey BG, O'Connor TP, Luettich K, Flieder DB, Kaplan R, Crystal RG. Variability of antioxidant-related gene expression in the airway epithelium of cigarette smokers. Am J Respir Cell Mol Biol. 2003 29:331-43 and in Heguy A, Harvey BG, O'Connor TP, Hackett NR, Crystal RG. Sampling-dependent up-regulation of gene expression in sequential samples of human airway epithelial cells. Mol Med. 2003 9:200-8. These data are part of a study aimed at understanding how cigarette smoking modifies neuroendocrine cells, in which microarray analysis with TaqMan confirmation was used to assess airway epithelial samples obtained by fiberoptic bronchoscopy from 81 individuals (normal nonsmokers, normal smokers, smokers with early COPD and smokers with established COPD). Of 11 genes considered to be neuroendocrine cell-specific, only ubiquitin C-terminal hydrolase L1(UCHL1), a member of the ubiquitin proteasome pathway, was consistently upregulated in smokers compared to nonsmokers. Up-regulation of UCHL1 at the protein level was observed with immunohistochemistry of bronchial biopsies of smokers compared to nonsmokers. Interestingly, however, while UCHL1 expression was present only in neuroendocrine cells of the airway epithelium in nonsmokers, UCHL1 expression was also expressed in ciliated epithelial cells in smokers, an intriguing observation in light of recent observations that ciliated cells can are capable of transdifferentiating to other airway epithelium. In the context that UCHL1 is involved in the degradation of unwanted, misfolded or damaged proteins within the cell and is overexpressed in >50% of lung cancers, its overexpression in chronic smokers may represent an early event in the complex transformation from normal epithelium to overt malignancy.
Keywords: smokers vs non-smokers
 
Overall design comparison of gene expression in airway epithelial cells of the large airways of phenotypic normal smokers vs normal non-smokers
 
Contributor(s) Carolan B, Heguy A, Harvey B, Leopold P, Ferris B, Crystal R
Citation(s) 17108109
Submission date Jun 12, 2006
Last update date Jul 08, 2016
Contact name Yael Strulovici-Barel
E-mail(s) yas2003@med.cornell.edu
Organization name Weill Cornell Medical College
Department Department of Genetic Medicine
Lab Crystal
Street address 1300 York Avenue
City New York
State/province NY
ZIP/Postal code 10021
Country USA
 
Platforms (1)
GPL80 [Hu6800] Affymetrix Human Full Length HuGeneFL Array
Samples (44)
GSM114034 large airways, non-smoker 010119L, MAS5
GSM114035 large airways, non-smoker 010119R, MAS5
GSM114036 large airways, non-smoker 010316L, MAS5
This SubSeries is part of SuperSeries:
GSE5060 Airway epithelium, large and small airways, phenotypically normal smokers, non-smokers, early COPD and COPD
Relations
BioProject PRJNA104495

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Supplementary data files not provided
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