Preliminary study on E-cadherin expression in dexamethasone-induced palatal cleft in mouse

Abstract

The glucocorticoid dexamethasone (DEX) can induce palatal cleft; however, the mechanism involved remains unclear. E-cadherin is an important cell adhesion molecule, and it can significantly affect cell fate and embryonic development. Recent studies have indicated that E-cadherin expression in palatal epithelial cells is suppressed in normal palate fusion. This study aimed to determine whether the change in E-cadherin expression is related to the incidence of cleft palate in DEX-induced mice. Mice were divided into the experimental group and the control group. Pregnant mice were injected with DEX on E10.0-E12.0, whereas mice in the control group were injected with normal saline. Hematoxylin and eosin (HE) staining, immunohistochemistry, and real-time quantitative polymerase chain reaction were employed to evaluate the effect of DEX on fetal mouse palatal processes, particularly the changes in E-cadherin and β-catenin expression levels in the phases of the experimental and control groups. Data indicated that the incidence of cleft palate in the DEX group was 43.59% (17/39), whereas that in the control group was only 3.03% (1/33). The results of HE staining showed that the obviously shortened palatal processes could not contact and fuse with one another in the DEX-treated mice model compared with those in the control group. The ectopic expression of E-cadherin in embryonic palatal mesenchymal cells was also analyzed. The expression levels of E-cadherin and β-catenin in the experimental group were higher than those in the control group. These findings indicated that DEX could induce E-cadherin gene upregulation and ectopic expression, as well as high β-catenin expression, thereby inhibiting the growth of mesenchyme cells and cleft palate.