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Upregulation of cellular retinoic acid‐binding protein I expression by ethanol
Author(s) -
Bi Jing,
Hu Xinli,
Zhou Feng C.,
Wei LiNa
Publication year - 2001
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1046/j.1440-169x.2001.00591.x
Subject(s) - retinoic acid , downregulation and upregulation , gene expression , regulation of gene expression , biology , ethanol , microbiology and biotechnology , gene , endocrinology , biochemistry
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.