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1 Physiology Program, Department of Environmental Health, Harvard School of Public Health; 2 Pulmonary and Critical Care Division, Department of Medicine, Brigham and Women's Hospital; and 3 Departments of Surgery and Pathology, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115
Airway smooth muscle
constriction leads to the development of compressive stress on
bronchial epithelial cells. Normal human bronchial epithelial cells
exposed to an apical-to-basal transcellular pressure difference
equivalent to the computed stress in the airway during
bronchoconstriction demonstrate enhanced phosphorylation of
extracellular signal-regulated kinase (ERK). The response is pressure
dependent and rapid, with phosphorylation increasing 14-fold in 30 min,
and selective, since p38 and c-Jun NH2-terminal kinase
phosphorylation remains unchanged after pressure application. Transcellular pressure also elicits a ninefold increase in expression of mRNA encoding heparin-binding epidermal growth factor-like growth
factor (HB-EGF) after 1 h, followed by prominent
immunostaining for pro-HB-EGF after 6 h. Inhibition of the ERK
pathway with PD-98059 results in a dose-dependent reduction in
pressure-induced HB-EGF gene expression. The magnitude of the HB-EGF
response to transcellular pressure and tumor necrosis factor (TNF)-
(1 ng/ml) is similar, and the combined mechanical and inflammatory
stimulus is more effective than either stimulus alone. These results
demonstrate that compressive stress is a selective and potent activator
of signal transduction and gene expression in bronchial epithelial cells.
mechanotransduction; airway; asthma; remodeling; mechanical stress
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