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Am J Physiol Lung Cell Mol Physiol 278: L1264-L1272, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 6, L1264-L1272, June 2000

Molecular responses of rat tracheal epithelial cells to transmembrane pressure

Barbara Ressler1, Richard T. Lee2, Scott H. Randell3, Jeffrey M. Drazen4, and Roger D. Kamm1

1 Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge 02139; 3 Division of Pulmonary and Critical Care Medicine and 4 Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts 02115; and 2 Cystic Fibrosis/ Pulmonary Research and Treatment Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599

Smooth muscle constriction in asthma causes the airway to buckle into a rosette pattern, folding the epithelium into deep crevasses. The epithelial cells in these folds are pushed up against each other and thereby experience compressive stresses. To study the epithelial cell response to compressive stress, we subjected primary cultures of rat tracheal epithelial cells to constant elevated pressures on their apical surface (i.e., a transmembrane pressure) and examined changes in the expression of genes that are important for extracellular matrix production and maintenance of smooth muscle activation. Northern blot analysis of RNA extracted from cells subjected to transmembrane pressure showed induction of early growth response-1 (Egr-1), endothelin-1, and transforming growth factor-beta 1 in a pressure-dependent and time-dependent manner. Increases in Egr-1 protein were detected by immunohistochemistry. Our results demonstrate that airway epithelial cells respond rapidly to compressive stresses. Potential transduction mechanisms of transmembrane pressure were also investigated.

asthma; gene expression; mechanical stress; early growth response-1; endothelin-1; transforming growth factor-beta 1


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