Periostin and matrix stiffness combine to regulate myofibroblast differentiation and fibronectin synthesis during palatal healing

摘要: Abstract Although the matricellular protein periostin is prominently upregulated in skin and gingival healing, it plays contrasting roles myofibroblast differentiation matrix synthesis respectively. Palatal healing associated with scarring that can alter or restrict maxilla growth, but expression pattern contribution of palatal unknown. Using periostin-knockout (Postn−/−) wild-type (WT) mice, to was investigated through 1.5 mm full-thickness excisional wounds hard palate. In WT 6 days post-wounding, mRNA levels peaking at day 12. Genetic deletion significantly reduced wound closure rates compared mice. Absence pivotal genes repair, including α-SMA/acta2, fibronectin βigh3. Recruitment fibroblasts inflammatory cells, as visualized by immunofluorescent staining for fibroblast specific factor-1, vimentin, macrophages markers Arginase-1 iNOS also impaired Postn−/−, not isolated from palate mice were cultured on collagen gels prefabricated silicon substrates varying stiffness. Postn−/− showed a ability contract gel, which rescued exogenous addition recombinant periostin. As stiffness increased, increasingly differentiated into myofibroblasts, same degree WT. Pharmacological inhibition Rac deficient myofibroblastic phenotype cells. Low (0.2 kPa) resulted upregulation an effect Quantification immunostaining vinculin integrinβ1 adhesions revealed Periostin required formation focal fibrillar mPFBs. Our results suggest modulates contraction via integrinβ1/RhoA pathway, ECM dependent manner healing.