Cytokeratin, vimentin and E-cadherin immunodetection in the embryonic palate in two strains of mice with different susceptibility to glucocorticoid-induced clefting.
An immunohistochemical study analyzing the pattern of distribution of some intermediate filament proteins, keratin and vimentin and, one adhesion molecule, cadherin in different stages of developing secondary palate in two strains 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 cleft palate (C57/BL). The heads of embryos were processed by standard immunohistochemistry with antipancytokeratin (KAE1), antikeratins 18 (K18) and 19 (K19), antivimentin, and anti E-cadherin antibodies. Immunostaining with KAE1 antibody showed differences between the strains. The reaction was stronger 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 processes and K18 and K19 showed no reaction in either strain of mice. Anti E-cadherin antibody was detected in the medial palatal epithelium of both strains of mice and in all stages of palate development. No differences were observed 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 palate in the mouse. The decreased immunoreaction of cytokeratins observed in the resistant strain would facilitate the disappearance of this molecule during the transformation from an epithelial to a mesenchymal phenotype that takes place during the development of the palate. These results may be related to the loss of cytokeratin expression observed during epithelial-mesenchymal transformation in the embryonic palate.
Montenegro
M A
MA
Department of Morphology, Biomedical Ciencies Institute, Faculty of Medicine, University of Chile. mmontene@machi.med.uchile.cl
Rojas
M
M
Dominguez
S
S
Vergara
A
A
D000818:Animals; D015820:Cadherins / Q000096:biosynthesis*; D004848:Epithelium / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D005938:Glucocorticoids / Q000494:pharmacology*; D007150:Immunohistochemistry; D007633:Keratins / Q000096:biosynthesis* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010159:Palate / Q000196:embryology* / Q000378:metabolism*; D013045:Species Specificity; D013997:Time Factors; D014746:Vimentin / Q000096:biosynthesis*
D015820:Cadherins; D005938:Glucocorticoids; D014746:Vimentin; D007633:Keratins