PTH1R signalling regulates the mechanotransduction process of cementoblasts under cyclic tensile stress.

Objective: To investigate the regulatory role of type I parathyroid hormone receptor (PTH1R) signalling in the mechanotransduction process of cementoblasts under cyclic tensile stress (CTS). Materials and methods: Immortalized cementoblast cell line OCCM-30 were employed and subjected to cyclic tensile strain applied by a four-point bending system. The expression of PTHrP and PTH1R, as well as cementoblastic transcription factor Runx-2, Osterix, and extracellular matrix protein COL-1 and OPN were assessed by quantitative real-time polymerase chain reaction and western blot analysis. PTH1R expression was knocked down by siPTH1R transfection, and the alteration of cementoblastic biomarkers expression was examined to evaluate the function of PTH1R. Furthermore, to investigate possible downstream molecules, expression of signal molecule ERK1/2 with or without siPTH1R transfection, and the effect of ERK inhibitor PD98059 on the expression of cementoblastic biomarkers was also examined. Results: Cyclic tensile strain elevated the expression of PTHrP and PTH1R, as well as cementoblastic biomarkers Runx-2, Osterix, COL-1, and OPN in a time-dependent manner, which was inhibited by siPTH1R transfection.The expression of phosphorylated ERK1/2 was upregulated time-dependently under cyclic stretch, which was also inhibited by siPTH1R transfection, and pretreatment of p-ERK1/2 inhibitor PD98059 undermined the increase of Runx-2, Osterix, COL-1, and OPN prominently. Conclusion: The findings of the present study indicate that PTH1R signalling plays a regulatory role in the CTS induced cementoblastic differentiation in mature cementoblasts, and ERK1/2 is essentially involved as a downstream intracellular signal molecule in this mechanotransduction process.