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Am J Physiol Lung Cell Mol Physiol 280: L705-L715, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 4, L705-L715, April 2001

FGF-10 disrupts lung morphogenesis and causes pulmonary adenomas in vivo

Jean C. Clark1, Jay W. Tichelaar1, Susan E. Wert1, Nobuyuki Itoh2, Anne-Karina T. Perl1, Mildred T. Stahlman3, and Jeffrey A. Whitsett1

1 Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039; 2 Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto 606-8501, Japan; and 3 Department of Pediatrics, Vanderbilt University, Nashville, Tennessee 37232-2370

Transgenic mice in which fibroblast growth factor (FGF)-10 was expressed in the lungs of fetal and postnatal mice were generated with a doxycycline-inducible system controlled by surfactant protein (SP) C or Clara cell secretory protein (CCSP) promoter elements. Expression of FGF-10 mRNA in the fetal lung caused adenomatous malformations, perturbed branching morphogenesis, and caused respiratory failure at birth. When expressed after birth, FGF-10 caused multifocal pulmonary tumors. FGF-10-induced tumors were highly differentiated papillary and lepidic pulmonary adenomas. Epithelial cells lining the tumors stained intensely for thyroid transcription factor (TTF)-1 and SP-C but not CCSP, indicating that FGF-10 enhanced differentiation of cells to a peripheral alveolar type II cell phenotype. Withdrawal from doxycycline caused rapid regression of the tumors associated with rapid loss of the differentiation markers TTF-1, SP-B, and proSP-C. FGF-10 disrupted lung morphogenesis and induced multifocal pulmonary tumors in vivo and caused reversible type II cell differentiation of the respiratory epithelium.

fibroblast growth factor; conditional expression


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