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Originally published In Press as doi:10.1074/jbc.M202253200 on April 1, 2002

J. Biol. Chem., Vol. 277, Issue 25, 22743-22749, June 21, 2002
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Fibroblast Growth Factor 18 Influences Proximal Programming during Lung Morphogenesis*

Jeffrey A. WhitsettDagger §, Jean C. ClarkDagger , Lara PicardDagger , Jay W. TichelaarDagger , Susan E. WertDagger , Nobuyuki Itoh, Anne-Karina T. PerlDagger , and Mildred T. Stahlman||

From the Dagger  Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039,  Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto 606-8501, Japan, and || Department of Pediatrics, Vanderbilt University, Nashville, Tennessee 37232-2370

The structure and functions of the airways of the lung change dramatically along their lengths. Large-diameter conducting airways are supported by cartilaginous rings and smooth muscle tissue and are lined by ciliated and secretory epithelial cells that are involved in mucociliary clearance. Smaller peripheral airways formed during branching morphogenesis are lined by cuboidal and squamous cells that facilitate gas exchange to a network of fine capillaries. The factors that mediate formation of these changing cell types and structures along the length of the airways are unknown. We report here that conditional expression of fibroblast growth factor (FGF)-18 in epithelial cells of the developing lung caused the airway to adopt structural features of proximal airways. Peripheral lung tubules were markedly diminished in numbers, whereas the size and extent of conducting airways were increased. Abnormal smooth muscle and cartilage were found in the walls of expanded distal airways, which were accompanied by atypically large pulmonary blood vessels. Expression of proteins normally expressed in peripheral lung tubules, including SP-B and pro-SP-C, was inhibited. FGF-18 mRNA was detected in normal mouse lung in stromal cells surrounding proximal airway cartilage and in peripheral lung mesenchyme. Effects were unique to FGF-18 because expression of other members of the FGF family had different consequences. These data show that FGF-18 is capable of enhancing proximal and inhibiting peripheral programs during lung morphogenesis.

* This work was supported by National Institutes of Health Grants HL56387 and HL41496, Cystic Fibrosis Research and Development Center from the Cystic Fibrosis Foundation, and The Francis Families Foundation (J. W. T.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed: Divisions of Neonatology and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave., Cincinnati, OH 45229-3039. Tel.: 513-636-4830; Fax: 513-636-7868; E-mail: jeff.whitsett@chmcc.org.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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