Mechanical loading activates β-catenin signaling in periodontal ligament cells

To determine whether β-catenin signaling is responsive to mechanical loading in periodontal ligament (PDL) cells.

To determine whether Wnt/β-catenin signaling pathway components are present and functional, PDL cells were treated with lithium chloride or Wnt3a-conditioned media. To determine whether mechanical strain activates β-catenin signaling, PDL cells were subjected to compressive loading. Activation of the β-catenin signaling pathway was determined by immunofluorescence, Western immunoblotting, and TOPflash assay.

Mimicking Wnt signaling stimulates β-catenin nuclear translocation and T-cell factor/lymphoid enhancer binding factor-dependent transcriptional activation in PDL cells. Mechanical loading stimulates a transient accumulation of dephosphorylated β-catenin in the cytoplasm and its translocation to the nucleus. This effect of strain acts through activation of protein kinase B and phosphorylation of glycogen synthase kinase-3 beta. These strain-related changes do not involve the low-density lipoprotein receptor-related protein 5/Wnt receptor.

The Wnt/β-catenin signaling pathway components are functional and activated by mechanical loading in PDL cells. β-catenin serves as an effector of mechanical signals in PDL cells.