The Study Of The Effect Of Hydrostatic Compress On The Viability And Apoptosis Of Condylar Chondrocytes And The Integrin/FAK Pathway

Objective Reduced mechanical stimuli such as hemimastication and limited masticatory movements,can significantly affect the metabolic activity of mandibular condylar chondrocytes and the growth of mandibles.However,the molecular mechanisms for these phenomena remain unclear.In this study,we hypothesized that integrin-FAK-ERK/PI3K signaling pathway mediated the cellular response of condylar chondrocytes to mechanical loading.Methods Primary condylar chondrocytes were exposed to hydrostatic compressive forces(HCFs)of different magnitudes(0,50,100,150,200 and 250 kPa)for 2 h.We measured the viability,morphology,and apoptosis of the chondrocytes with different treatments as well as the gene,protein expression,and phosphorylation of mechanosensitivity-related molecules,such as integrina2,integrinα5,integrinβ1,FAK,ERK,andPI3KResults HCFs could significantly increase the viability and surface area of condylar chondrocytes and decrease their apoptosis in a dose-dependent manner.HCF of 250 kPa resulted in a 1.51±0.02-fold increase of cell viability and reduced the ratio of apoptotic cells from 18.10%±0.56%to 7.30%±1.43%.HCFs could significantly enhance the mRNA and protein expression of integrina2,integrinα5,and integrinβ1 in a dose-dependent manner,but not ERK1,ERK2 or PI3K.Instead,HCF could significantly increase phosphorylation levels of FAK,ERK1/2and PI3K in a dose-dependent manner.Cilengitide,the potent integrin inhibitor,could dose-dependently block such effects of HCFs.Conclusion HCFs ranging from 50kPa to 250 kPa could enhances the viability and decreases the apoptosis;HCFs could affect the viability and apoptosis of condylar chondrocytes through the integrin-FAK-ERK/PI3K pathway.