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Am J Physiol Lung Cell Mol Physiol 277: L1205-L1213, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 6, L1205-L1213, December 1999

TGF-beta 3-null mutation does not abrogate fetal lung maturation in vivo by glucocorticoids

Wei Shi1, Nora Heisterkamp2, John Groffen2, Jingsong Zhao3, David Warburton1,3, and Vesa Kaartinen1

1 Developmental Biology Program and 2 Section of Molecular Carcinogenesis, Childrens Hospital Los Angeles and University of Southern California School of Medicine, Los Angeles 90027; and 3 Center for Craniofacial Molecular Biology, University of Southern California School of Medicine and Dentistry, Los Angeles, California 90033

Newborn transforming growth factor (TGF)-beta 3-null mutant mice exhibit defects of palatogenesis and pulmonary development. Glucocorticoids, which play a central role in fetal lung maturation, have been postulated to mediate their stimulatory effects on tropoelastin mRNA expression through TGF-beta 3 in cultured lung fibroblasts. In the present study, we analyzed the abnormally developed lungs in TGF-beta 3-null mutant mice and compared the effects of glucocorticoids on gene expression and lung morphology between TGF-beta 3 knockout and wild-type mice. Lungs of TGF-beta 3-null mutant mice on embryonic day 18.5 did not form normal saccular structures and had a thick mesenchyme between terminal air spaces. Moreover, the number of surfactant protein C-positive cells was decreased in TGF-beta 3-null mutant lungs. Interestingly, glucocorticoids were able to promote lung maturation and increased expression of both tropoelastin and fibronectin but decreased the relative number of surfactant protein C-positive cells in fetal lungs of both genotypes. This finding provides direct evidence that glucocorticoid signaling in the lung can use alternative pathways and can exert its effect without the presence of TGF-beta 3.

transforming growth factor-beta 3; tropoelastin expression


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