Strain increases airway smooth muscle contractile and cytoskeletal
proteins in vitro.
Smith, P. G., R. Moreno, M. Ikebe.
Department of Pediatrics and Department of Physiology and
Biophysics, Case Western Reserve University School of Medicine,
Cleveland, Ohio
APStracts 3:0154L, 1996.
Mechanical stress contributes to lung development and the progression
of some lung diseases though 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 independent
of other in vivo influences. Cultured canine ASM cells were subjected
to two levels of cyclic deformational strain for 14 days and compared
to non-strained cells by SDS-PAGE and Western blotting. Cells
subjected to 16-30% strain demonstrated increases in total cellular
protein, myosin, myosin light chain kinase (MLCK) and desmin while
the cellular contents of actin, vimentin and tubulin were similar.
Changes in myosin appeared mostly due to the SMI smooth muscle
isoform while non-muscle 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 independent
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.
Received 19 March 1996; accepted in final form 21 August 1996.
APS Manuscript Number L87-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996