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Series GSE5058 Query DataSets for GSE5058
Status Public on Nov 21, 2006
Title Airway epithelium, small airways, normal non-smokers, phenotypic normal smokers, smokers with COPD and early COPD
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 39 HG-U133 Plus 2.0 GeneChips, from 12 normal non-smokers, 12 phenotypic normal smokers, 9 Early COPD and 6 COPD individuals, all small airways, all small airway. A subset of these samples have been already submitted under GEO Accession Number GSE 4498. These are: 12 non-smokers samples (GSM101095-GSM101106) and 10 smoker samples (GSM101107-GSM101116). These 22 samples that are also in GSE4498 were described in Harvey, B-G; Heguy, A.; Leopold, P.L.; Carolan, B.; Ferris, B. and Crystal R.G. Modification of Gene Expression of the Small Airway Epithelium in Response to Cigarette Smoking. J. Mol. Med (in press). 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: non-smokers vs phenotypic normal smokers, smokers with early COPD, and smokers with COPD
 
Overall design comparison of gene expression in airway epithelial cells of the small airways of normal non-smokers, phenotypic normal smokers, smokers with early COPD and smokers with COPD
 
Contributor(s) Carolan B, Heguy A, Harvey B, Leopold P, Ferris B, Crystal R
Citation(s) 17108109, 19106307
Submission date Jun 12, 2006
Last update date Mar 25, 2019
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)
GPL570 [HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array
Samples (39)
GSM101095 small airways, non-smoker 001, RMA and MAS
GSM101096 small airways, non-smoker 004, RMA and MAS
GSM101097 small airways, non-smoker 002, RMA and MAS
This SubSeries is part of SuperSeries:
GSE5060 Airway epithelium, large and small airways, phenotypically normal smokers, non-smokers, early COPD and COPD
Relations
BioProject PRJNA104499

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE5058_RAW.tar 809.0 Mb (http)(custom) TAR (of CEL, CHP)
Processed data provided as supplementary file

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