Focal adhesion kinase mediates ß-catenin signaling in periodontal ligament cells.
Biochem Biophys Res Commun
; 439(4): 487-92, 2013 Oct 04.
Article
em En
| MEDLINE
| ID: mdl-24021281
ABSTRACT
Periodontal ligament (PDL) cells convert the orthodontic forces into biological responses by secreting signaling molecules to induce modeling of alveolar bone and tooth movement. Beta-catenin pathway is activated in response to mechanical loading in PDL cells. The upstream signaling pathways activated by mechanical loading resulting in the activation of ß-catenin pathway through Wnt-independent mechanism remains to be characterized. We hypothesized that mechanical loading induces activation of ß-catenin signaling by mechanisms that dependent on focal adhesion kinase (FAK) and nitric oxide (NO). We found that mechanical or pharmacological activation of ß-catenin signaling in PDL cells upregulated the expression of ß-catenin target genes. Pre-treatment of PDL cells with FAK inhibitor-14 prior to mechanical loading abolished the mechanical loading-induced phosphorylation of Akt and dephosphorylation of ß-catenin. PDL cells pre-treated with NO donor or NO inhibitor and subjected to mechanical loading. Western blot analysis showed that the mechanical loading or pre-treatment with NO donor increased the levels of dephosphorylated ß-catenin, pAkt, and pGSK-3ß. Pre-treatment with NO inhibitor blocked the mechanical loading-induced phosphorylation of Akt and dephosphorylation of ß-catenin. These data indicate that mechanical loading-induced ß-catenin stabilization in PDL cells involves phosphorylation of Akt by two parallel pathways requiring FAK and NO.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Ligamento Periodontal
/
Transdução de Sinais
/
Proteína-Tirosina Quinases de Adesão Focal
/
Beta Catenina
Idioma:
En
Ano de publicação:
2013
Tipo de documento:
Article