p120 regulates E-cadherin expression in nasal epithelial cells in chronic rhinosinusitis.

BACKGROUND: The epithelial barrier plays an important role in the regulation of immune homeostasis. The effect of the immune environment on E-cadherin has been demonstrated in previous studies. This discovery prompted new research on the targeting mechanism of E-cadherin in chronic rhinosinusitis (CRS). METHODS: E-cadherin and p120 expression was determined by quantitative RT-PCR, and western blot. The interaction between E-cadherin and p120 was assessed by immunofluorescence staining and coimmunoprecipitation assays. Human nasal epithelial cells (HNECs) were cultured with submerged methods and transfected with p120-specific small interfering RNA. In other experiments, HNECs differentiated with the air-liquid interface (ALI) method were stimulated with various cytokines and Toll-like receptor (TLR) agonists. The barrier properties of differentiated HNECs were determined by assessing fluorescent dextran permeability. RESULTS: E-cadherin and p120 expression was decreased in HNECs from patients with CRS, and the p120 protein expression level was positively correlated with that of E-cadherin. Two isoforms of p120 (p120-1 and p120-3) were expressed in HNECs, with p120-3 being the main isoform. Knocking down p120 in HNECs cultured under submerged conditions significantly reduced the E-cadherin protein expression. The Rac1 inhibitor NSC23766 reversed the protein expression of E-cadherin in p120 knockdown experiments. Inflammatory mediators, including IL-4, TNF-α, TGF- ß, LPS and IFN-Î, reduced E-cadherin and p120 protein expression and increased paracellular permeability. Dexamethasone abolished the downregulation of E-cadherin and p120 caused by inflammatory mediators. CONCLUSIONS: p120 is involved in regulating E-cadherin protein expression in CRS. Dexamethasone may alleviate the reduction in E-cadherin and p120 protein expression caused by inflammatory mediators.

Alveolar ridge augmentation with bioactive glass ceramics: a histological study.

A particulate BGC (bioactive glass ceramics), has been developed as a new bone graft biomaterial for alveolar ridge augmentation and has been evaluated by simulated animal models. Five beagle dogs were used in this investigation. Prior to augmentation the mandibular posterior teeth of the animals were extracted. Three months after the extractions, the porous BGC particles were packed into the subperiosteal tunnels in the ridges with a special syringe. The animals were killed at different time intervals and the specimens were examined by light microscopy, scanning electron microscopy (SEM), and X-ray energy dispersive analysis (EDAX), respectively. The results of this study indicate that the BGC particles are firmly combined with the adjacent hard and soft tissues by the bone bonding interface between the implants and the alveolar bone, and by the ingrowth of bone or fibrous connective tissue into the interspaces and the pores of the particles. The results have demonstrated that particulate BGC with pores is an excellent implant material for alveolar ridge augmentation because of its very good biocompatibility.