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