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1 Meakins Christie Laboratories, McGill University, Montreal, Quebec, Canada
2 Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA
3 Genetics Unit, Shriner's Hospital for Crippled Children, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: mara.ludwig{at}mcgill.ca.
Decorin, a small leucine-rich proteoglycan with a widespread tissue distribution, is required for the normal fibrillogenesis of collagen in most tissues. As collagen is important in determining the elastic behaviour of the lung, we hypothesized that lung tissue mechanics would be altered in a mutant mouse in which the single decorin gene was abrogated by targeted deletion (Dcn-/-). Complex impedence of the respiratory system (ZRS) was measured in C57Bl/6 mice, (Dcn -/- and Dcn+/+) using a small animal ventilator which delivers a volume signal with multiple frequencies to the trachea. A constant phase model was fit to calculate airway resistance (Raw), tissue damping and tissue elastance. Compliance (CRS) was measured from a pressure volume curve during stepwise deflations. Lungs were excised and parenchymal tissue strips mounted in an organ bath for in vitro measurement of tissue impedence (Ztis) and quasistatic length-stress curves. In addition, pulmonary tissue was examined by immunohistochemistry and immunoblotting. In vivo, in the Dcn-/- mice, Raw was decreased and CRS increased. Similarly, in vitro, length-stress curves showed increased Ctis in the Dcn-/- mice. These alterations in lung tissue mechanical behaviour in Dcn-/- mice support a critical role for decorin in the formation of the lung collagen network..
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