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J Appl Physiol 101: 1127-1135, 2006. First published June 1, 2006; doi:10.1152/japplphysiol.01287.2005
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Polyamine-mediated reduction in human airway epithelial migration in response to wounding is PGE2 dependent through decreases in COX-2 and cPLA2 protein levels

Mark J. Cowan,1 Timothy Coll,1 and James H. Shelhamer2

1Department of Medicine, Division of Pulmonary and Critical Care Medicine, The University of Maryland School of Medicine, Baltimore, and 2Critical Care Medicine Department, The National Institutes of Health, Bethesda, Maryland

Submitted 6 October 2005 ; accepted in final form 29 May 2006

Both ornithine decarboxylase inhibition to deplete polyamines and cyclooxygenase inhibition diminish the migration response to injury of human airway epithelial cells in tissue culture monolayers by ~75%. Restoration of normal migration responses is achieved in the polyamine depleted system either by exogenous reconstitution of polyamines or the addition of prostaglandin E2 (PGE2). However, only PGE2 was able to restore migration in the cyclooxygenase-inhibited systems. Western blot for cyclooxygenase-2 and cytosolic phospholipase A2 protein levels and ELISAs for PGE2 secretion demonstrate dramatic increases over 24–48 h after monolayer wounding. These increases are completely abolished by polyamine depletion or cyclooxygenase inhibition. We conclude that polyamine inhibition decreases cellular migration in response to injury in airway epithelial cells at least in part through inhibiting normal PGE2 production in response to injury. This may be brought about by decreases in cytosolic phospholipase A2 and cyclooxygenase-2 protein levels.

ornithine decarboxylase; putrescine, spermidine; spermine; restitution; airway epithelial cell; prostaglandin E2; cytosolic phospholipase A2; cyclooxygenase; asthma; chronic obstructive pulmonary disease


Address for reprint requests and other correspondence: M. J. Cowan, Dept. of Medicine, The Univ. of Maryland, 10 North Greene St., Rm. 3D122, Baltimore, MD 21201 (e-mail: mcowan{at}medicine.umaryland.edu)






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