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

Pediatr Res. 1999 Jan;45(1):2-7. 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Dexamethasone / pharmacology*
  • Down-Regulation
  • Gene Expression Regulation / drug effects*
  • Glucocorticoids / pharmacology*
  • Lung / drug effects
  • Lung / growth & development
  • Lung / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Retinoic Acid / genetics*
  • Retinol-Binding Proteins / genetics*
  • Retinol-Binding Proteins, Cellular
  • Tretinoin / pharmacology*
  • Up-Regulation


  • Glucocorticoids
  • Rbp1 protein, rat
  • Receptors, Retinoic Acid
  • Retinol-Binding Proteins
  • Retinol-Binding Proteins, Cellular
  • retinoic acid binding protein I, cellular
  • Tretinoin
  • Dexamethasone