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1 Departments of Physiology and 2 Surgery, Faculty of Medicine, University of Manitoba, Manitoba, Winnipeg R3E 3J7; and 3 Unité de recherche en pneumologie, Centre de recherche de Hôpital Laval, Institut universitaire de cardiologie et pneumologie, Université Laval, Québec, Canada G1V 4G5
Whether contractility of
bronchial smooth muscle cells (BSMC) from asthmatic subjects is
significantly altered has never been validated. We tested the
hypothesis that such BSMC show increased contractility. Cells were
isolated from endobronchial biopsies. BSMC shortening was measured
under an inverted microscope. Statistically significant increases in
maximum shortening capacity (
Lmax) and velocity (Vo) were found in asthmatic BSMC
compared with normal cells. Mean Lmax in
asthmatic BSMC was 39.05 ± 1.99% (SE) of resting cell length
compared with 28.6 ± 1.1% in normal cells; mean
Vo was 7.2 ± 0.8% of resting cell
length/s in asthmatic cells and 5.23 ± 0.46% in normal cells. To
investigate the mechanism of the increased contractility, we measured
mRNA abundance of smooth muscle types of myosin light chain kinase
(smMLCK) and myosin heavy chain. RT-PCR data revealed that smMLCK mRNA
was higher in asthmatic BSMC (0.106 ± 0.021 arbitrary
densitometric units, n = 7) than in control cells
(0.04 ± 0.008, n = 11; P < 0.05). Messages for myosin heavy chain isoforms showed no difference. Increased kinase message content is an index of the mechanism for the
increased velocity and capacity of shortening we report.
asthmatic bronchial smooth muscle contractility; smooth muscle myosin light chain kinase; single bronchial smooth muscle cell mechanics; single bronchial smooth muscle cell biochemistry
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