Gene expression of cellular retinoid-binding proteins : Modulation by retinoic acid and dexamethasone in postnatal rat lung

• Published in: Pediatric research Vol. 45; no. 1; pp. 2 - 7
• Main Authors: WHITNEY, D, MASSARO, G. D, MASSARO, D, CLERCH, L. B
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 1999
• Subjects: Animals; Biological and medical sciences; Dexamethasone - pharmacology; Down-Regulation; Embryology: invertebrates and vertebrates. Teratology; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - drug effects; Glucocorticoids - pharmacology; Lung - drug effects; Lung - growth & development; Lung - metabolism; Organogenesis. Fetal development; Organogenesis. Physiological fonctions; Rats; Rats, Sprague-Dawley; Receptors, Retinoic Acid - genetics; Retinol-Binding Proteins - genetics; Retinol-Binding Proteins, Cellular; Tretinoin - pharmacology; Up-Regulation; Corticosteroid; Dexamethasone; Rat; Lung; Rodentia; Retinoid; Gene expression; Postnatal development; Biological activity; Binding protein; Vertebrata; Regulation(control); Mammalia; Pulmonary alveolus; Newborn animal; Animal; Modulation; Retinoic acid
• ISSN: 0031-3998; 1530-0447
• DOI: 10.1203/00006450-199901000-00002

In rats, septation of gas-exchange saccules occurs during the first 2 postnatal weeks; dexamethasone (DEX) treatment irreversibly impairs septation, and treatment with all-trans retinoic acid (RA) prevents the DEX-induced inhibition of septation. Cellular retinoic acid-binding protein I (CRABP I) and cellular retinol-binding protein I (CRBP I) are important modulators of the cellular metabolism of retinoids. In the present study, therefore, we measured the mRNA concentration of CRABP I and CRBP I in lungs of neonatal rats. In untreated rats, CRABP I and CRBP I mRNA peaked at postnatal d 8, indicating that CRABP I and CRBP I are developmentally regulated at least in part at a pretranslational level during lung septation. Daily treatment of 3- to 8-d-old rats with RA (500 microg/kg/d) had no effect on the level of CRABP I mRNA; treatment with DEX (0.25 microg/d) from d 4 to 8 caused a decrease in CRABP I mRNA that was not prevented by concomitant treatment with RA. These findings suggest that a decrease in CRABP I expression may be important in the DEX-induced block of septation but not in the prevention by RA of DEX-induced inhibition of septation. RA treatment caused an increase of CRBP I mRNA; conversely, treatment with DEX caused a decrease in CRBP I mRNA that was prevented by concomitant treatment with RA. These data suggest CRBP I may play a role in RA-induced septation, in the inhibition of septation caused by DEX, and in the ability of RA to prevent DEX-blocked septation.