HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Woodruff, P. G. Search for Related Content PubMed PubMed Citation Articles by Woodruff, P. G.

Gene Expression in Asthmatic Airway Smooth Muscle

¹ Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, San Francisco, California

Correspondence and requests for reprints should be addressed to Prescott G. Woodruff, M.D., M.P.H., Department of Medicine, Division of Pulmonary and Critical Care Medicine, and Cardiovascular Research Institute, University of California, San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143-0111. E-mail: prescott.woodruff{at}ucsf.edu

ABSTRACT

Airway smooth muscle abnormalities are central to the pathophysiology of asthma. These airway smooth muscle cell abnormalities may include changes in cell number, size, phenotype, or function. Gene expression studies performed using asthmatic airway smooth muscle cells represent one approach to identifying the abnormalities of airway smooth muscle that occur in asthma in vivo. However, due to the technical challenges involved, only two studies have been performed to date using freshly obtained tissue from subjects with asthma. The first of these studies suggested increased expression of myosin light-chain kinase in airway smooth muscle from patients with asthma, whereas the second study found no difference in myosin light-chain kinase expression, nor any difference in other markers of smooth muscle phenotype in asthma. Studies performed in cell culture through the application of gene expression microarrays to profile airway smooth muscle cells exposed to potential mediators of asthma yield more consistent results, including induction by IL-13 of tenascin, the H1 histamine receptor, and IL-13 receptor subunits. However, the significance of these microarray findings for smooth muscle function is uncertain. Furthermore, gene expression studies have a fundamental limitation in that many functional properties of airway smooth muscle are regulated at other levels (e.g., protein phosphorylation). Thus, gene expression studies ultimately must be integrated with other methodological approaches to adequately study airway smooth muscle in asthma in vivo.

Key Words: airway smooth muscle • gene expression, microarray • polymerase chain reaction