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.