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. 2011 Dec 3;67(6):477–487. doi: 10.1136/thoraxjnl-2011-200508

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© 2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

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Induction of urokinase plasminogen activator receptor (uPAR) is a feature of primary bronchial epithelial cell (NHBEC) wound repair in an air–liquid interface (ALI) differentiated model. Wound repair in differentiated NHBECs occurs over 24 h (representative of n=2). (A) uPAR expression is increased in cells at the wound edge 4 h after wounding (arrows). uPAR (B, E), urokinase plasminogen activator (uPA) (C, F) and plasminogen activator inhibitor 1 (PAI-1) (D, G) mRNA and protein levels in supernatants were measured in wounded and unwounded cells over 24 h. Matrix metalloproteinase 9 (MMP-9) (H) and plasmin (I) activity were measured at 24 h. *p<0.05, **p<0.01, ***p<0.001.