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Articles in PresS, published online ahead of print February 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00396.2001
Submitted on October 11, 2001
Accepted on February 12, 2002
1 Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA
2 Division of Pulmonary Medicine, University Hospital, Bern, Switzerland
3 Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA; Department of Anesthesia, University of California, San Francisco, San Francisco, CA, USA
4 Division of Pulmonary and Critical Care Medicine, University of California, Los Angeles, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: lware{at}mednet.ucla.edu.
Pretreatment with keratinocyte growth factor (KGF) ameliorates experimentally-induced acute lung injury in rats. Though alveolar epithelial type II cell hyperplasia probably contributes, the mechanisms underlying KGF's protective effect remain incompletely described. Therefore, we tested the hypothesis that KGF given to rats in vivo would enhance alveolar epithelial repair in vitro by non-proliferative mechanisms. 48h after intratracheal instillation of KGF (5mg/kg), alveolar epithelial type II cells were isolated for in vitro alveolar epithelial repair studies. KGF treated cells had markedly increased epithelial repair (96 ± 22%)compared with control cells (p < 0.001). KGF treated cells had increased cell spreading and migration at the wound edge, but no increase in in vitro proliferation compared to control cells. KGF treated cells were more adherent to extracellular matrix proteins and polystyrene. Inhibition of the EGF receptor with tyrosine kinase inhibitors abolished the KGF effect on epithelial repair. In conclusion, in vivo administration of KGF augments the epithelial repair rate of alveolar epithelial cells by altering cell adherence, spreading, and migration and through stimulation of the EGF receptor.
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