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Am J Physiol Lung Cell Mol Physiol (December 14, 2001). doi:10.1152/ajplung.00371.2001
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Articles in PresS, published online ahead of print December 14, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00371.2001
Submitted on September 19, 2001
Accepted on December 8, 2001

Fusion of Lung Lobes and Vessels in Mouse Embryos Heterozygous for the Forkhead Box f1Targeted Allele

Lorena Lim1, Kalinichenko V Vladimir1, Jeffrery A Whitsett2, and Robert H Costa1*

1 Molecular Genetics, University of Illinois at Chicago, Chicago, IL, USA
2 Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, OH, USA

* To whom correspondence should be addressed. E-mail: robcosta{at}uic.edu.

Previously, we showed that newborn Foxf1 +/- mice with diminished pulmonary Foxf1 levels died of severe lung hemorrhage and exhibited abnormal formation of alveolar sacs and capillaries. Another group recently reported that Foxf1 +/- mouse embryos displayed a number of organ and skeletal defects including fusion of lung lobes. However, identification of pulmonary genes whose altered expression was associated with the lobular fusion defect in Foxf1 +/- lungs remains uncharacterized. The present study was conducted to determine the nature of the malformations leading to lung fusions in the Foxf1 embryos and to identify potential signaling pathways influenced by Foxf1 haploinsufficiency. We show that Foxf1 +/- embryos exhibit defects in formation and branching of primary lung buds, causing fusion of the right lung lobes and vessels. The severity of the Foxf1 +/- lung fusions was correlated with decreased levels of Foxf1 mRNA. In situ hybridization studies demonstrated that the defective primary lung bud development in early Foxf1 +/- embryos was associated with fewer pulmonary mesenchymal-epithelial interfaces. Defects in branching morphogenesis in the Foxf1 +/- embryos were associated with altered expression of the Fgf10, Bmp4 and Gli3 transcription factor, which are known to influence primary lung bud development.




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