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Am J Physiol Lung Cell Mol Physiol 281: L250-L257, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 1, L250-L257, July 2001

Novel mechanisms in murine nitrofen-induced pulmonary hypoplasia: FGF-10 rescue in culture

Juan M. Acosta1,2,*, Bernard Thébaud3,4,5,6,*, Carmenza Castillo2, Arnaud Mailleux3, Denise Tefft2, Carol Wuenschell2, Kathryn D. Anderson1, Jacques Bourbon7, Jean-Paul Thiery3, Savério Bellusci3, and David Warburton1,2,3

1 Division of Pediatric Surgery and Developmental Biology Program, Childrens Hospital Los Angeles Research Institute, Keck School of Medicine, University of Southern California, Los Angeles 90027; 2 The Center for Craniofacial Molecular Biology, University of Southern California School of Dentistry, Los Angeles, California 90033; 3 Equipe Morphogénèse Cellulaire et Progression Tumorale, Institut Curie Unité Mixte de Recherche 144 Centre National de la Recherche Scientifique, 75005 Paris; 4 Service de Pédiatrie et Réanimation Néonatales-UPRES EA2704, Hôpital Antoine Béclère, 92141 Clamart; 5 Service de Physiologie Respiratoire, Hôpital Cochin, Université René Descartes, 75005 Paris; 6 Vascular Biology Research Group, University of Alberta, Edmonton, Alberta T6G 2S2, Canada; and 7 Institut National de la Santé et de la Recherche Médicale Unité 319, Universite Jussieu, 75005 Paris, France

We evaluated the role of the key pulmonary morphogenetic gene fibroblast growth factor-10 (Fgf10) in murine nitrofen-induced primary lung hypoplasia, which is evident before the time of diaphragm closure. In situ hybridization and competitive RT-PCR revealed a profound disturbance in the temporospatial pattern as well as a 10-fold decrease in mRNA expression level of Fgf10 but not of the inducible inhibitor murine Sprouty2 (mSpry2) after nitrofen treatment. Exogenous FGF-10 increased branching not only of control lungs [13% (right) and 27% (left); P < 0.01] but also of nitrofen-exposed lungs [23% (right) and 77% (left); P < 0.01]. Expression of mSpry2 increased 10-fold with FGF-10 in both nitrofen-treated and control lungs, indicating intact downstream FGF signaling mechanisms after nitrofen treatment. We conclude that nitrofen inhibits Fgf10 expression, which is essential for lung growth and branching. Exogenous FGF-10 not only stimulates FGF signaling, marked by increased mSpry2 expression, in both nitrofen-treated and control lungs but also substantially rescues nitrofen-induced lung hypoplasia in culture.

congenital diaphragmatic hernia; lung hypoplasia; fibroblast growth factor-10; murine Sprouty2

* Juan M. Acosta and Bernard Thébaud contributed equally to this work.




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