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Am J Physiol Lung Cell Mol Physiol (December 30, 2005). doi:10.1152/ajplung.00397.2005
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Submitted on September 15, 2005
Accepted on December 21, 2005

Desmin modulates lung elastic recoil and airway responsiveness

Felix R Shardonofsky1*, Yassemi Capetanaki2, and Aladin M Boriek3

1 Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas, USA
2 Department of Cell Biology, Baylor College of Medicine, Houston, Texas, USA
3 Department of Medicine, Baylor College of Medicine, Houston, Texas, USA

* To whom correspondence should be addressed. E-mail: felix.shardonofsky{at}utsouthwestern.edu.

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 P-V 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 (H) 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.




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