Retinoic acid and dexamethasone affect RAR-β and surfactant protein C mRNA in the MLE lung cell line
| Autor: | Mary A. Grummer, Richard D. Zachman |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Pulmonary and Respiratory Medicine
medicine.medical_specialty Transcription Genetic Receptors Retinoic Acid Physiology Proteolipids Retinoic acid Tretinoin Cycloheximide Biology Dexamethasone Cell Line Mice chemistry.chemical_compound Pulmonary surfactant Physiology (medical) Internal medicine polycyclic compounds medicine Animals RNA Messenger Lung Messenger RNA Pulmonary Surfactants Surfactant protein C Cell Biology Molecular biology Kinetics Endocrinology Gene Expression Regulation chemistry Cell culture Dactinomycin hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 274:L1-L7 |
| ISSN: | 1522-1504 1040-0605 |
| Popis: | 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-β (5.5 times) and SP-C (2 times) mRNA, with maximal effects at 24 h and at 10−6M. 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-β mRNA, but SP-C mRNA degradation was slowed, indicating an effect on SP-C mRNA stability. Dex decreased RAR-β and SP-C expression to 75 and 70% of control values, respectively, with greatest effects at 48 h and at 10−7M. There was no effect of Dex on either RAR-β or SP-C mRNA disappearance with actinomycin D. However, cycloheximide prevented the effect of Dex. Despite Dex, RA increased both RAR-β and SP-C mRNA. This work suggests that RA and Dex affect RAR-β and SP-C genes by different mechanisms. |
| Databáze: | OpenAIRE |
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