JNK Signaling Pathway Mediates Fluoride-Induced Upregulation of CK1 α during Enamel Formation

This study aimed to investigate the effects of fluoride on CK1α expression and to assess the regulation of molecular signaling involving fluoride a nd CK1α during enamel development. Kunming mice were randomly divided into the control and F groups with induced clinical features of fluorosis. The F group mice, including mothers and newborns, were treated with 50 ppm fluoridated water. Immunohistochemical staining of the sections of the embryoni c mandible regions was performed at the bell stage. Protein expression and signaling pathways in a mouse-derived ameloblast-like cell line (LS8) exposed to fluoride or a Jun N-terminal kinase (JNK) inhibitor were compared to those in control cells without exposure. CK1α and proteins of the JNK sign aling pathways were assayed by quantitative real-time PCR and Western blotting. Mice of the F group developed dental fluorosis. Scanning electron microscopy showed a significant reduction in the degree of mineralization in the F group mice, which manifested as thin, loosely arranged, and disorganize d enamel rods. Additional analysis revealed that the expression of CK1α in the F group was significantly elevated compared with that in the control group; LS8 cells responded to fluoride by upregulation of CK1α expression through the JNK pathway. Our findings identified the potential effects of CK 1α on fluorosis using a mouse model and revealed that a high fluoride level increases the expression of CK1α and that JNK can be a key regulatory...

Source: Caries Research - April 7, 2021 Category: Dentistry Source Type: research