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Departments of Pediatrics, Vanderbilt University School of Medicine Nashville, Tennessee 37232-2370
Biochemistry, Vanderbilt University School of Medicine Nashville, Tennessee 37232-2370
Address all correspondence and requests for reprints to: Margaret G. Rush, M.D., Department of Pediatrics, Vanderbilt University School of Medicine, A-0126 MCN, Nashville, Tennessee 37232-2370.
Abstract
Cellular retinol-binding protein (CRBP) is a potential mediator of vitamin A action. To determine whether retinoic acid and dexamethasone administration, alone and in combination, influence CRBP gene expression, adult female vitamin A-sufficient Sprague-Dawley rats randomly received 1) all-trans retinoic acid (100 µg) by intragastric intubation, 2) dexamethasone (2 µg/g BW) by ip injection, or 3) both all-trans retinoic acid and dexamethasone in the same doses. Control animals received either cottonseed oil by intragastric intubation or saline by ip injection. Six hours after treatment, lung and liver tissue were collected for Northern blot analysis with the radiolabeled cDNA specific for rat CRBP. Retinoic acid administration increased the amount of lung CRBP mRNA only, whereas dexamethasone decreased both lung and liver CRBP mRNA abundance. In animals treated with both retinoic acid and dexamethasone, CRBP mRNA abundance was also reduced. We conclude that CRBP gene expression can be modulated by both retinoic acid and dexamethasone in the vitamin A-sufficient animal. In the whole animal, our findings indicate that dexamethasone not only represses CRBP gene expression, but also opposes the effect of retinoic acid.
Footnotes
* Presented at the Annual Meeting of the Society for Pediatric Research, May 1990. This work was supported by Grants DK-26657, HL-07256, HL-14214, and HD-09195 from the NIH.
Received March 11, 1991.
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