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Am J Physiol Lung Cell Mol Physiol 274: L1-L7, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 1, L1-L7, January 1998

Retinoic acid and dexamethasone affect RAR-beta and surfactant protein C mRNA in the MLE lung cell line

Mary A. Grummer1 and Richard D. Zachman1,2

Departments of 1 Pediatrics and 2 Nutritional Sciences, Meriter Hospital Perinatal Center, University of Wisconsin, Madison, Wisconsin 53715

Lung development and surfactant biosynthesis are affected by retinoic acid (RA) and dexamethasone (Dex). Using a mouse lung epithelial cell line, we are exploring RA-Dex interactions through the study of RA and Dex effects on RA receptor (RAR) and surfactant protein (SP) C mRNA expression. RA increased expression of RAR-beta (5.5 times) and SP-C (2 times) mRNA, with maximal effects at 24 h and at 10-6 M. The RA induction was not inhibited by cycloheximide, suggesting RA affects transcription. With added actinomycin D, RA did not affect the disappearance rate of RAR-beta mRNA, but SP-C mRNA degradation was slowed, indicating an effect on SP-C mRNA stability. Dex decreased RAR-beta and SP-C expression to 75 and 70% of control values, respectively, with greatest effects at 48 h and at 10-7 M. There was no effect of Dex on either RAR-beta or SP-C mRNA disappearance with actinomycin D. However, cycloheximide prevented the effect of Dex. Despite Dex, RA increased both RAR-beta and SP-C mRNA. This work suggests that RA and Dex affect RAR-beta and SP-C genes by different mechanisms.

gene expression; type II cells; steroid hormone superfamily; lung development; vitamin A; messenger ribonucleic acid


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