Wnt3a signaling induces murine dental follicle cells to differentiate into cementoblastic/osteoblastic cells via an osterix‐dependent pathway

Abstract

These findings suggest that HERS has a potential role in stimulating cementoblast/osteoblast differentiation of dental follicle cells via the Wnt/β-catenin signaling pathway.

Wnt5a attenuates Wnt3a-induced alkaline phosphatase expression in dental follicle cells

“…It was noted that treatment with siWnt5a as well as the addition of rWnt5a had no significant effect on the proliferative response compared with that in the respective control (data not shown), indicating that the inhibitory effects of rWnt5a were not a reflection of alterations in the cell number. On the other hand, the expression of the Osx gene, which was reported to be upregulated by Wnt3a [18], was not significantly affected by the addition of 100 ng/ml rWnt5a (Fig. 3D).…”

“…dental follicle cells, regarded as precursor cells of cementoblasts [17]. Furthermore, we have recently reported that the expression of Wnt3a was detected on HERS [18], which is considered to have an inductive role in initiating root formation by epithelial-mesenchymal interaction. On the other hand, we have reported the opposite effect of Wnt3a for highly differentiated cementoblasts by showing that canonical Wnt/β-catenin signaling stimulated by rWnt3a inhibits the cementoblastic differentiation of murine immortalized cementoblasts, OCCM30, with reduced gene expression levels of ALP, Runx2, and Osx [19].…”

“…Canonical Wnt/β-catenin signaling has been shown to enhance cementoblast differentiation in vivo using mouse models [14][15][16] and to induce rat dental follicle cells to differentiate into cementoblastic/osteoblastic-type cells in vitro [17]. Recently, we detected the expression of Wnt3a on HERS during mouse tooth root development [18]. These findings led us to examine the role of Wnt5a signaling in the canonical Wnt/β-catenin-mediated cementoblastic/osteoblastic differentiation of SVF4.…”

“…Recent studies in vivo have reported that constitutive stabilization of β-catenin in dental mesenchyme leads to excessive cementum formation [14,15], and that disruption of Wnt/β-catenin signaling in dental mesenchyme arrests the differentiation of cementoblasts [16], suggesting that canonical Wnt/β-catenin signaling is required for cementum formation. In addition, studies in vitro have demonstrated that Wnt/β-catenin signaling up-regulates differentiation and proliferation in rat/mouse dental follicle cells [17,18] and murine cementoblasts [19], respectively, suggesting the involvement of Wnt/β-catenin signaling in cementogenesis.…”

Role of the Wnt signaling molecules in the tooth

“…In immortalized murine dental follicle cells, Wnt3a induced ALP expression. Moreover, Wnt3a induced Runx2 and Osterix in these cells, suggesting a potential role of HERS in stimulating cementoblast/osteoblast differentiation of dental follicle cells via the canonical Wnt signaling pathway [63]. The activation of the canonical Wnt signaling has recently been reported to induce in vivo cementum regeneration in the rat periodontal defect model and in vitro cementoblast differentiation of human periodontal ligament cells [64].…”