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Gestational exposure to ethanol suppresses msx2 expression in developing mouse embryos

L Rifas1, D A Towler, L V Avioli

  • 1Department of Internal Medicine, Divisions of Bone and Mineral Diseases and Molecular Pharmacology, Washington University School of Medicine and Barnes-Jewish Hospital North, St. Louis, MO 63110, USA. lrifas@imgate.wustl.edu

Proceedings of the National Academy of Sciences of the United States of America
|July 8, 1997
PubMed
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Ethanol exposure in pregnant mice significantly reduced msx2 gene expression in developing embryos and fetal cells. This inhibition of msx2 may explain developmental abnormalities seen in fetal alcohol syndrome.

Area of Science:

  • Developmental biology
  • Teratology
  • Molecular genetics

Background:

  • Ethanol is a known teratogen causing fetal abnormalities.
  • msx2 is a gene crucial for skeletal and craniofacial development.

Purpose of the Study:

  • To investigate if ethanol-induced teratogenicity involves the dysregulation of msx2 gene expression.
  • To examine the effect of ethanol on msx2 expression during embryonic development.

Main Methods:

  • Exposure of pregnant mice to ethanol on embryonic day 8.
  • Whole mount in situ hybridization to detect msx2 expression in E11-11.5 embryos.
  • Reverse transcription-PCR and Northern blot analysis on fetal osteoblastic cells exposed to ethanol.
  • Analysis of msx2 promoter activity in osteoblasts.

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Main Results:

  • Ethanol-exposed embryos were smaller and lacked msx2 expression in key developmental structures.
  • msx2 expression was reduced by 40-50% in fetal osteoblastic cells treated with ethanol.
  • Alkaline phosphatase activity increased twofold in ethanol-exposed osteoblasts.
  • Ethanol suppressed msx2 promoter activity in osteoblasts.

Conclusions:

  • Fetal alcohol exposure decreases msx2 expression, a regulator of osteoblast and myoblast differentiation.
  • Inhibition of msx2 expression is a potential mechanism underlying developmental retardation, craniofacial defects, and cardiac abnormalities in fetal alcohol syndrome.