Cytokeratin, vimentin and E-cadherin immunodetection in the embryonic palate in two strains of mice with different susceptibility to glucocorticoid-induced clefting

Citation
Ma. Montenegro et al., Cytokeratin, vimentin and E-cadherin immunodetection in the embryonic palate in two strains of mice with different susceptibility to glucocorticoid-induced clefting, J CRAN GENE, 20(3), 2000, pp. 137-143
Citations number
30
Categorie Soggetti
Molecular Biology & Genetics
Journal title
JOURNAL OF CRANIOFACIAL GENETICS AND DEVELOPMENTAL BIOLOGY
ISSN journal
02704145 → ACNP
Volume
20
Issue
3
Year of publication
2000
Pages
137 - 143
Database
ISI
SICI code
0270-4145(200007/09)20:3<137:CVAEII>2.0.ZU;2-K
Abstract
An immunohistochemical study analyzing the pattern of distribution of some intermediate filament proteins, keratin and vimentin and, one adhesion mole cule, cadherin in different stages of developing secondary palate in two st rains of mice with different H-2 backgrounds was undertaken to investigate differences between a strain that is susceptible to glucocorticoid-induced cleft palate (A/Sn) and one that is resistant to glucocorticoid-induced cle ft palate (C57/BL). The heads of embryos were processed by standard immunoh istochemistry with antipancytokeratin (KAE1), antikeratins 18 (K18) and 19 (K19), antivimentin, and anti E-cadherin antibodies. Immunostaining with KA E1 antibody showed differences between the strains. The reaction was strong er in the medial edge epithelia of palatal processes in the A/Sn strain at all stages of palatogenesis. The C57/BL strain showed a weak immunostain to KAE1. Antivimentin antibody stained the mesenchymal cells of palatal proce sses and K18 and K19 showed no reaction in either strain of mice. Anti E-ca dherin antibody was detected in the medial palatal epithelium of both strai ns of mice and in all stages of palate development. No differences were obs erved in E-cadherin and vimentin immunostain in palatal epithelium between the strains. The different expression of some cytokeratins in the embryonic palatal epithelium suggests that these intermediate filament proteins may be involved in different susceptibility to glucocorticoid-induced cleft pal ate in the mouse. The decreased immunoreaction of cytokeratins observed in the resistant strain would facilitate the disappearance of this molecule du ring the transformation from an epithelial to a mesenchymal phenotype that takes place during the development of the palate. These results may be rela ted to the loss of cytokeratin expression observed during epithelial-mesenc hymal transformation in the embryonic palate.