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Genetic Differences in Airway Smooth Muscle Function

¹ Department of Medicine, Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada

Correspondence and requests for reprints should be addressed to James G. Martin, B.Sc., M.B. B.Ch., M.D., Meakins-Christie Laboratories, Department of Medicine, McGill University, 3626 St. Urbain Street, Montréal, PQ, H2X 2P2 Canada. E-mail: james.martin{at}mcgill.ca

ABSTRACT

The genetic basis for airway smooth muscle properties is poorly explored. Contraction and relaxation are altered in asthmatic airway smooth muscle, but the basis for the alterations and the role that muscle-specific susceptibility genes may play is largely unexplored. Alterations in the β-adrenergic receptor, signaling pathways affecting inositol phosphate metabolism, adenylyl and guanylyl cyclase activity, and contractile proteins such as the myosin heavy chain are all suggested by experimental model systems. Significant changes in proliferative and secretory capacities of asthmatic smooth muscle are also demonstrated, but their genetic basis also requires elucidation. Certain asthma-related genes such as ADAM33, although potentially important for smooth muscle function, have been incompletely explored.

Key Words: airway responsiveness • F344 rats • A/J mice • β-adrenergic receptors • myosin isoforms