title: Gene expression of cellular retinoid-binding proteins: modulation by retinoic acid and dexamethasone in postnatal rat lung.
abstract: 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.
authors.affiliation: Department of Pediatrics, Georgetown University School of Medicine, Washington, DC 20007, USA.
authors.forename: D
authors.initials: D
authors.lastname: Whitney
authors.forename: G D
authors.initials: GD
authors.lastname: Massaro
authors.forename: D
authors.initials: D
authors.lastname: Massaro
authors.forename: L B
authors.initials: LB
authors.lastname: Clerch
mesh_terms: D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology*; D015536:Down-Regulation; D005786:Gene Expression Regulation / Q000187:drug effects*; D005938:Glucocorticoids / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018168:Receptors, Retinoic Acid / Q000235:genetics*; D012177:Retinol-Binding Proteins / Q000235:genetics*; D054840:Retinol-Binding Proteins, Cellular; D014212:Tretinoin / Q000494:pharmacology*; D015854:Up-Regulation
chemical_list: D005938:Glucocorticoids; C518458:Rbp1 protein, rat; D018168:Receptors, Retinoic Acid; D012177:Retinol-Binding Proteins; D054840:Retinol-Binding Proteins, Cellular; C082927:retinoic acid binding protein I, cellular; D014212:Tretinoin; D003907:Dexamethasone