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Am J Physiol Lung Cell Mol Physiol 290: L890-L896, 2006. First published December 30, 2005; doi:10.1152/ajplung.00397.2005
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Desmin modulates lung elastic recoil and airway responsiveness

Felix R. Shardonofsky,1 Yassemi Capetanaki,2 and Aladin M. Boriek3

1Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas; 2Division of Cell Biology, Center of Basic Research, Academy of Athens, Athens, Greece; and 3Department of Medicine, Baylor College of Medicine, Houston, Texas

Submitted 15 September 2005 ; accepted in final form 21 December 2005

Desmin is a structural protein that is expressed in smooth muscle cells of both airways and alveolar ducts. Therefore, desmin could be well situated to participate in passive and contractile force transmission in the lung. We hypothesized that desmin modulates lung compliance, lung recoil pressure, and airway contractile response. To test this hypothesis, respiratory system complex impedance (Zin,rs) at different positive end-expiratory pressure (PEEP) levels and quasi-static pressure-volume data were obtained in desmin-null and wild-type mice at baseline and during methacholine administration. Airways and lung tissue properties were partitioned by fitting Zin,rs to a constant-phase model. Relative to controls, desmin-null mice showed 1) lower values for lung stiffness and recoil pressure at baseline and induced airway constriction, 2) greater negative PEEP dependence of H and airway resistance under baseline conditions and cholinergic stimulation, and 3) airway hyporesponsiveness. These results demonstrate that desmin is a load-bearing protein that stiffens the airways and consequently the lung and modulates airway contractile response.

compliance; hysteresis; airway resistance


Address for reprint requests and other correspondence: F. R. Shardonofsky, Univ. of Texas Southwestern Medical Center, Dept. of Pediatrics, 5323 Harry Hines Blvd., Dallas, TX 75390-9063 (e-mail: felix.shardonofsky{at}utsouthwestern.edu)




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