West China Journal of Stomatology ›› 2008, Vol. 26 ›› Issue (05): 546-549.

Previous Articles     Next Articles

Spatial and temporal changes of palatal cell proliferation and cell apoptosis of retinoic acid induced mouse cleft palate in different embryonic stages

WANG Ru1, LIU Bin2, WANG Bo2, CONG Wei2, XIAO Jing2   

  1. 1. Dept. of Stomatology, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China; 2. Dept. of Basic Oral Science, College of Stomatology, Dalian Medical University, Dalian 116044, China
  • Received:2008-10-25 Revised:2008-10-25 Online:2008-10-20 Published:2008-10-20
  • Contact: XIAO Jing,Tel:0411-86110400

Abstract:

Objective To study the effect of retinoic acid(RA) on cell proliferation and apoptosis of palatal shelves by 5 -bromo -2 -deoxyuridine(BrdU) and terminal -deoxynucleotidyl transferase mediated nick end labeling (TUNEL). Methods C57BL/6J mice were used to establish the RA induced cleft palate animal model, in which the pregnant mice were given a single dose of RA at 100 mg/kg body weight on gestation day 10(GD10) and GD12, respectively. Specimens were prepared for immunohistochemical staining by using BrdU and TUNEL monoclonal antibodies. Results The percentages of BrdU positive cells of embryonic palatal mesenchyme(EPM) and medial edge epithelium(MEE) in GD10 RA group were both obviously lower than that of control group. There was no difference between GD12 RA group and control group. Abnormally intense staining of TUNEL was detected in the palatal mesenchymal cells of GD10 day RA group but not in control group and GD12 day RA group. Conclusion After exposure of embryonic mice to RA on GD10, the proliferation and apoptosis of palatal mesenchymal cells are increased, this causes the smaller size of shelves and failure of fusion. The MEE cells keep a bilayer midline epithelial seam after exposure on GD12 with normal apoptosis, this indicates that cell apoptosis in MEE cells be not the only process required for palatal fusion.

Key words: cleft palate, retinoic acid, cell proliferation, cell apoptosis