AJP - Lung Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 282: L169-L182, 2002; doi:10.1152/ajplung.00243.2001
1040-0605/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (21)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Banerjee, S. K.
Right arrow Articles by Blackburn, M. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Banerjee, S. K.
Right arrow Articles by Blackburn, M. R.
Vol. 282, Issue 2, L169-L182, February 2002

EDITORIAL FOCUS
Gene expression profiling in inflammatory airway disease associated with elevated adenosine

Suman K. Banerjee, Hays W. J. Young, Jonathan B. Volmer, and Michael R. Blackburn

Department of Biochemistry and Molecular Biology, University of Texas-Houston Medical School, Houston, Texas 77030

Adenosine has been implicated as a modulator of inflammatory processes central to asthma. However, the molecular mechanisms involved are poorly understood. We used Atlas mouse cDNA arrays to analyze differential gene expression in association with lung inflammation resulting from elevated adenosine in adenosine deaminase (ADA)-deficient mice. We report that of the 1,176 genes on the array, the expression patterns of 280 genes were consistently altered. Of these genes, the steady-state levels of 93 genes were upregulated and 29 were downregulated. We also show that lowering adenosine levels with ADA enzyme therapy has striking effects on gene expression that may be associated with resolution of pulmonary eosinophilia. In addition, we confirmed the nucleic acid and protein expression of vascular endothelial growth factor and monocyte chemoattractant protein-3, two candidate genes that may be regulated by adenosine. In conclusion, high-throughput profiling of gene expression by cDNA array hybridization has provided an overview of critical regulatory genes involved in airway inflammation in ADA-deficient mice. These mice will serve as a useful in vivo model for characterizing molecular mechanisms of adenosine-mediated lung damage.

complementary deoxyribonucleic acid; adenosine deaminase; vascular endothelial growth factor; monocyte chemoattractant protein-3


This article has been cited by other articles:


Home page
 Am. J. Respir. Cell Mol. Bio.Home page
H. W. J. Young, C.-X. Sun, C. M. Evans, B. F. Dickey, and M. R. Blackburn
A3 Adenosine Receptor Signaling Contributes to Airway Mucin Secretion after Allergen Challenge
Am. J. Respir. Cell Mol. Biol., November 1, 2006; 35(5): 549 - 558.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. Roman, H. N. Rivera, S. Roser-Page, S. V. Sitaraman, and J. D. Ritzenthaler
Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling
Am J Physiol Lung Cell Mol Physiol, February 1, 2006; 290(2): L317 - L325.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
S. T. Holgate
Adenosine: a key effector molecule of asthma or just another mediator?
Am J Physiol Lung Cell Mol Physiol, February 1, 2002; 282(2): L167 - L168.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online