Periostin-integrin interaction regulates force-induced TGF-β1 and α-SMA expression by hPDLSCs

Objective: Periostin (PN), a major matricellular periodontal ligament (PDL) protein, modulates the remodeling of the PDL and bone, especially under mechanical stress. This study investigated the requirement of PN-integrin signaling in force-induced expression of transforming growth factor-beta 1 (TGF-β1) and alpha-smooth muscle actin (α-SMA) in human PDL stem cells (hPDLSCs). Methods: Cells were stimulated with intermittent compressive force (ICF) using computerized controlled apparatus. Cell migration was examined using in vitro scratch assay. The mRNA expression was examined using real-time polymerase chain reaction. The protein expression was determined using immunofluorescent staining and western blot analysis. Results: Stimulation with ICF for 24 h increased the expression of PN, TGF-β1, and α-SMA, along with increased SMAD2/3 phosphorylation. Knockdown of POSTN (PN gene) decreased the protein levels of TGF-β1 and pSMAD2/3 upon force stimulation. POSTN knockdown of hPDLSCs resulted in delayed cell migration, as determined by a scratch assay. However, migration improved after seeding these knockdown cells on pre-PN-coated surfaces. Further, the knockdown of αVβ5 significantly attenuated the force-induced TGF-β1 expression. Conclusion: Our findings indicate the importance of PN-αVβ5 interactions in ICF-induced TGF-β1 signaling and the expression of α-SMA. Findings support the critical role of PN in maintaining the PDL's tissue integrity and homeostasis.