[Inhibition of pSmad implicated in cleft palate induced by all-trans retinoic acid]

Wei Sheng Yan Jiu. 2009 Mar;38(2):136-8.
[Article in Chinese]

Abstract

Objective: To investigate the effects of excessive all-trans retinoic acid (atRA) on palatogenesis in mouse fetuses and level of Smad2 phophorylation (pSmad2).

Methods: atRA (80 mg/kg x d) was orally given to mice on embryonic day 11 (E11). Palatal fusion was examined by Hemagglutinin Esterase (HE). The level of Smad2 phophorylation (pSmad2) in medial edge epithelial (MEE) was detected by immunohistochemistry and Western Blot, respectively.

Results: The incidence of cleft palate (CP) was 90% of total fetus in atRA-treated group. Compared with vehicle control group, no pSmad2 was identified in MEE in atRA-treated palatal shelves, which was correlated with the persistence of the MEE and failure of palatal fusion.

Conclusion: Inhibition of Smad phosphorylation might be involved in cleft palate induced by atRA.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cleft Palate / chemically induced*
  • Female
  • Maternal Exposure / adverse effects*
  • Mice
  • Mice, Inbred ICR
  • Phosphorylation
  • Pregnancy
  • Random Allocation
  • Signal Transduction / drug effects
  • Smad2 Protein / metabolism*
  • Tretinoin / toxicity*

Substances

  • Smad2 Protein
  • Smad2 protein, mouse
  • Tretinoin