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Series GSE36174 Query DataSets for GSE36174
Status Public on Mar 01, 2012
Title LPS-induced expression in rat lung epithelial cells
Organism Rattus norvegicus
Experiment type Expression profiling by array
Summary Acute lung inflammation can alter the pulmonary function of susceptible individuals and exacerbate the pathogenesis of chronic inflammatory lung diseases including chronic obstructive pulmonary disease (COPD), cystic fibrosis and asthma. Exposure to lipopolysaccharide (LPS) or endotoxin, a constituent of outer cell membrane of gram negative bacteria, induces airway inflammation that is primarily characterized by increased polymorphonuclear neutrophils (PMNs) at early time points. Because LPS is present in variety of occupational and home environments and is an active constituent of cigarette smoke it is a risk factor for increasing prevalence and severity of non-occupational COPD, for adult onset of asthma and for wheezing in children. In airway epithelial cells, LPS stimulation increases mucin gene expression and mucous production. Hypersecretion of mucus overwhelms the ciliary clearance and obstructs airways, causing morbidity and mortality in chronic inflammatory respiratory lung diseases. In addition, acute bacterial infection contributes to the exacerbation of chronic airway diseases, specifically in advanced COPD and CF subjects, leading to increased healthcare burden and higher mortality. Bcl-2, a prosurvival protein that inhibits cell death plays a key role in normal cellular homeostasis and regulates the integrity of the mitochondrial and endoplasmic reticulum membranes. Gain- and loss-of-function studies showed that Bcl-2 expression sustains hyperplastic epithelial cells, and Bcl-2 expression is elevated in airway epithelial cells of subjects with cystic fibrosis and asthma. The present study investigated which inflammatory mediators induce mucous cell metaplasia and Bcl-2 expression following LPS exposure. Microarray analyses of mRNA from airway epithelial cells captured by laser microdissection from rat lungs snap-frozen at day 0 and 2 post LPS exposure were analyzed.
Microarray analysis of mRNA from airway epithelial cells captured by laser microdissection from rat lungs snap-frozen at day 0 and day 2 post LPS exposure was performed to identify inflammatory mediators modulated by LPS exposure.
 
Overall design Specific pathogen-free F344/NCrR male rats of 8–10 wk of age (from NCI, Frederick, MD) were exposed to LPS (1000 ug in 0.5 ML Saline) and rats were sacrificed on day 0 and day 2 of LPS exposure. Right lungs were snap-frozen in OCT and airway epithelial cells were captured by laser-dissection microsopy to extract RNA. Gene expression data from nonexposed rats (0d) was used a control.
 
Contributor(s) Chen Y, Wright P
Citation(s) 22461702
Submission date Feb 29, 2012
Last update date Feb 21, 2017
Contact name Hitendra Chand
E-mail(s) hchand@lrri.org
Phone 505-348-8774
Organization name Lovelace Respiraotry Research Institute
Street address 2425 Ridgecrest Dr SE
City Albuquerque
State/province NM
ZIP/Postal code 87108
Country USA
 
Platforms (1)
GPL85 [RG_U34A] Affymetrix Rat Genome U34 Array
Samples (6)
GSM882304 Rat Lung at Day 0, biological rep1
GSM882306 Rat Lung at Day 0, biological rep2
GSM882307 Rat Lung at Day 0, biological rep3
Relations
BioProject PRJNA152911

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
GSE36174_RAW.tar 30.3 Mb (http)(custom) TAR (of CEL, CHP, TXT)
Raw data provided as supplementary file
Processed data included within Sample table
Processed data provided as supplementary file

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