Upregulation of cellular retinoic acid-binding protein I expression by ethanol

Jing Bi, Xinli Hu, Feng C. Zhou, Li-Na Wei

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Acute and chronic ethanol ingestion cause embryopathy similar to that of hyper- or hypovitaminosis A. Experimental data have suggested interaction between vitamin A and alcohol signaling pathways at the level of metabolic interference, which ultimately affects the concentration of retinoic acid (RA) in animals. The present study was set up to examine the possible effects of alcohol on cellular RA binding protein I (CRABP-I) expression during embryonic development by using transgenic mouse embryos and P19 embryonal carcinoma cells as experimental models. It was found that expression of the mouse CRABP-I gene was elevated in developing embryos at mid-gestation stages as a result of ethanol consumption by the mothers. Specific elevation of this gene was detected in the limb bud and the gut. In the P19 model, the CRABP-I gene was directly upregulated by ethanol, which was not blocked by a protein synthesis inhibitor. Furthermore, the regulation of the CRABP-I gene by ethanol was mediated by the 5′ upstream regulatory region of the CRABP-I gene promoter. A potential interaction of vitamin A and ethanol at the level of CRABP-I gene expression is discussed.

Original languageEnglish (US)
Pages (from-to)553-561
Number of pages9
JournalDevelopment Growth and Differentiation
Issue number5
StatePublished - 2001


  • Alcohol
  • Gene regulation
  • Transgenic mouse
  • Vitamin A
  • β-galactosidase


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