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

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).

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.

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.

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.