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Experimental Lung Research Volume 33, 2007 - Issue 8-9
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DURATION-DEPENDENT CYTOPROTECTIVE VERSUS INFLAMMATORY EFFECTS OF LUNG EPITHELIAL FIBROBLAST GROWTH FACTOR-7 EXPRESSION

Jay W. Tichelaar Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USACorrespondence[email protected]
,
Scott C. Wesselkamper Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
,
Supurna Chowdhury Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
,
Hulian Yin Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
,
Pierre-Yves Berclaz Division of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
,
Maureen A. Sartor Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
,
George D. Leikauf Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA; Department of Environmental and Occupational Health, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
&
Jeffrey A. Whitsett Divisions of Pulmonary Biology and Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
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Pages 385-417 | Received 20 Jul 2007, Accepted 17 Sep 2007, Published online: 02 Jul 2009
 
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Abstract

Fibroblast growth factor-7 (FGF7) is a lung epithelial cell mitogen that is cytoprotective during injury. Transgenic mice that conditionally expressed FGF7 were used to dissect the mechanisms of FGF7 protection during lung injury. FGF7 improved survival when induced 3 days prior to acute lung injury. In contrast, FGF7 caused pulmonary inflammation and lung injury after 7 days or longer. Gene expression analysis of mouse lung mRNA identified mRNAs that contribute to the protective effects of FGF7. FGF7 improved survival during acute lung injury in adult mouse lung after short-term expression, but paradoxically induced inflammation and injury after persistent expression.

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