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Published ahead of print on October 24, 2003, doi:10.1165/rcmb.2003-0236OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 5, May 2004, 613-619

A more recent version of this article appeared on May 1, 2004
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Submitted on June 18, 2003
Revised on October 23, 2003

Altered Epithelial Cell Proportions in the Fetal Lung of Glucocorticoid Receptor Null Mice

Timothy J Cole1*, Nicola M Solomon2, Rosemary Van Driel3, Julie A Monk1, Daniel Bird1, Samantha J Richardson1, Rodney J Dilley3, and Stuart B Hooper4

1 Biochemistry and Molecular Biology, University of Melbourne, Melbourne, Victoria, Australia, 2 Murdoch Children's Research Institute, Melbourne, Victoria, Australia, 3 Baker Heart Research Institute, Melbourne, Victoria, Australia, 4 Physiology, Monash University, Melbourne, Victoria, Australia

* To whom correspondence should be addressed. E-mail: tjcole{at}unimelb.edu.au.

Glucocorticoids provide important signals for maturation of the fetal lung and antenatal glucocorticoids are used to reduce the respiratory insufficiency suffered by preterm infants. To further understand the role of glucocorticoids in fetal lung maturation, we have analysed mice with a targeted null mutation for the glucocorticoid receptor (GR) gene, which severely retards lung development. The lungs of fetal GR null mice have increased lung weight and DNA content, are condensed, hypercellular, with reduced septal thinning leading to a six fold increase in the airway to capillary diffusion distance. In fetal GR null mice, mRNA levels of the type-II epithelial cell surfactant protein genes A and C were reduced by ~50%. Analysis of epithelial cell types by electron microscopy revealed that the proportions of type-II cells were increased by ~30% , whereas the proportions of type-I cells were markedly reduced (by ~50%). Similarly, we found a 50% reduction in mRNA levels for T1{alpha} and aquaporin -5, two type-I cell-specific markers and a 20% reduction in aquaporin-1 mRNA levels. This demonstrates that during murine embryonic development, receptor-mediated glucocorticoid signaling facilitates the differentiation of epithelial cells into type-I cells, but are not obligatory for type-II cell differentiation.




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