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1 Department of Pediatrics, Georgetown University School of Medicine, Washington, DC, USA
2 Department of Biology, Georgetown University School of Medicine, Washington, DC, USA
3 Center for Genetic Medicine, Children's National Medical Center, Washington, DC, USA
4 Department of Medicine, Georgetown University School of Medicine, Washington, DC, USA
* To whom correspondence should be addressed. E-mail: clerchlb{at}georgetown.edu.
Treatment of newborn mice with dexamethasone (Dex) inhibits the subdivision of lung saccules to form alveoli; treatment with all-trans retinoic acid (RA) prevents this inhibition of septation. To better understand the early molecular signals responsible for the effects of Dex and RA, Affymetrix gene profiling was done on RNA isolated from 4-day-old mice after treatment with 1) diluent, 2) RA (1mg/kg), 3) Dex (0.7 µg/pup), or 4) RA + Dex. Each sample was assayed in duplicate on U74Av2 GeneChips. Data were analyzed using Affymetrix suite 5.0, corrected for saturation, and evaluated using GeneSpring 5.1 software. Stringent filtering of data using the global error model and condition-to-condition comparisons was used to identify 46 genes demonstrating significantly different expression between the lungs of Dex and RA + Dex treated mice. A query of the gene ontology database revealed the major biological processes affected by treatment with Dex and RA were cell growth/maintenance and cellular communication. Based on microarray data analysis, we hypothesize that Dex-induced inhibition of septation is associated with a block in angiogenesis due to down-regulation of the kinase domain receptor (KDR), also known as VEGF receptor-2 (VEGFR-2) and fetal liver kinase (Flk-1), and that the down-regulation of KDR is prevented by treatment with RA.
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