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AJP - Lung Cellular and Molecular Physiology, Vol 272, Issue 1 20-L27, Copyright © 1997 by American Physiological Society
ARTICLES |
P. G. Smith, R. Moreno and M. Ikebe
Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
Mechanical stress contributes to lung development and the progression of some lung diseases, although its effects on individual lung cells are unknown. Because increased airway smooth muscle (ASM) is found in lung diseases where abnormal stress is present, we determined if strain (change in resting length) causes ASM hypertrophy independently of other in vivo influences. Cultured canine ASM cells were subjected to two levels of cyclic deformational strain for 14 days and compared with nonstrained cells by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting. Cells subjected to 16-30% strain demonstrated increases in total cellular protein, myosin, myosin light chain kinase (MLCK), and desmin, whereas the cellular contents of actin, vimentin, and tubulin were similar. Changes in myosin appeared mostly due to the smooth muscle isoform, whereas nonmuscle myosin was unchanged. The increases in myosin and MLCK were disproportionate to increases in total protein, suggesting selective changes in contractile proteins. These relative increases in content of proteins were not as pronounced with 0-16% strain, suggesting a graded response. These data suggest that strain per se can increase the contractile proteins of ASM cells independently of other in vivo factors and modulates cultured cell phenotype to a more differentiated state, since it increases smooth muscle-specific proteins, such as smooth muscle myosin isoforms and desmin.
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