Buor-Chang Wu

The Role of Integrin αv in Proliferation and Differentiation of Human Dental Pulp Cell Response to Calcium Silicate Cement

INTRODUCTION It has been proved that integrin αv activity is related to cell proliferation, differentiation, migration, and organ development. However, the biological functions of integrin αv in human dental pulp cells (hDPCs) cultured on silicate-based materials have not been explored. The aim of this study was to investigate the role of integrin αv in the proliferation and odontogenic differentiation of hDPCs cultured with the effect of calcium silicate (CS) cement and β-tricalcium phosphate (TCP) cement. METHODS In this study, hDPCs were cultured on CS and TCP materials, and we evaluated fibronectin (FN) secretion and integrin αv expression during the cell attachment stage. After small interfering RNA transfection targeting integrin αv, the proliferation and odontogenesis differentiation behavior of hDPCs were analyzed. RESULTS The results indicate that CS releases Si ion-increased FN secretion and adsorption, which promote cell attachment more effectively than TCP. The CS cement facilitates FN and αv subintegrin expression. However, the FN adsorption and integrin expression of TCP are similar to that observed in the control dish. Integrin αv small interfering RNA inhibited odontogenic differentiation of hDPCs with the decreased formation of mineralized nodules on CS. It also down-regulated the protein expression of multiple markers of odontogenesis and the expression of dentin sialophosphoprotein protein. CONCLUSIONS These results establish composition-dependent differences in integrin binding and its effectiveness as a mechanism regulating cellular responses to biomaterial surface.

Stem cell differentiation-induced calcium silicate cement with bacteriostatic activity

Calcium-based bone cements are widely used in dental and orthopaedic surgery. Those based on calcium phosphate (CPCs) or calcium silicate (CSCs) have a number of favourable properties that encourage their clinical use in bone defect repair. The purpose of the present study was to compare the in vitro osteogenesis and bacteriostatic activity of BoneSource CPCs with home-made CSCs, particularly in regard to their facility for cell differentiation. Cement in vitro osteogenic activity was evaluated by incubating the cement specimens with human mesenchymal stem cells (hMSCs). The bacteriostatic activity of the two cements against Gram-positive (S. aureus) and Gram-negative (P. aeruginosa) bacterial strains was assessed using a bacteriostasis ratio assay and by inhibition zone examination. Compared with CPC, CSC was shown to promote greater proliferation and osteogenic differentiation (alkaline phosphatase and osteocalcin), and the formation of mineralization nodules of hMSCs. It is worth noting that CSC could effectively induce hMSC differentiation, even when the culture medium did not contain osteogenetic differentiation agents. Compared with CPC, CSC also showed significantly greater bacteriostatic activity, as revealed by inhibition zones and the bacteriostasis ratio. Our findings suggest that CSC is a useful bioactive material for bone repair in terms of inducing cell differentiation, and may be considered an alternative to CPCs.

Comparative Osteogenesis of Radiopaque Dicalcium Silicate Cement and White-Colored Mineral Trioxide Aggregate in a Rabbit Femur Model

The radiopaque dicalcium silicate cement (RDSC) displayed a shortened setting time and good biocompatibility. This study aimed to compare the regenerative potential of RDSC and white-colored mineral trioxide aggregate (WMTA) using a rabbit femur model. The animals were sacrificed at one, three and six months to accomplish histological and biochemical analyses. The results indicated that after one month of implantation, WMTA was associated with a greyish color alteration within its mass, while RDSC presented color stability even at six months. Histological assay with Masson’s Trichrome and Von Kossa stains showed the presence of newly formed bone surrounding the implanted sites in the rabbit femur. The histochemical data revealed that the RDSC group had significantly more bone regeneration than did the WMTA groups at three and six months. The conclusion drawn is that the encouraging results support the potential applications of RDSC as an improved alternative to WMTA for endodontic uses.

Selaginella tamariscina extract suppresses TPA-induced invasion and metastasis through inhibition of MMP-9 in human nasopharyngeal carcinoma HONE-1 cells

BackgroundNasopharyngeal carcinoma (NPC) is known for its high incidence of neck lymph node metastasis, which represents poor prognosis. The present study aimed to examine the anti-metastatic properties of Selaginella tamariscina extract (STE) in human nasopharyngeal carcinoma HONE-1 cells in vitro.MethodsCell viability was examined by MTT assay, whereas cell motility was measured by invasive, migration and would healing assays. Real-time PCR, and promoter assays confirmed the inhibitory effects of STE on matrix metalloproteinase-9 (MMP-9) mRNA level in HONE-1 cells.ResultsThe STE inhibits 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced HONE-1 cell migration and invasion in a concentration-dependent manner. By zymographic and Western blot analyses, STE was shown to inhibit the activities and expression of MMP-9. Treatment of STE on TPA-induced HONE-1 cells inhibited MMP-9 expression and ERK1/2 phosphorylation without affecting JNK and p38 phosphorylation.ConclusionsSTE inhibits MMP-9 expression and HONE-1 cell metastasis. Its inhibitory effects may involve the Src/FAK/ERK 1/2 pathway. STE may have the potential of being an anti-metastatic agent against NPC.

Aspirin-induced inhibition of adipogenesis was p53-dependent and associated with inactivation of pentose phosphate pathway.

Obesity has become a major public health problem of global significance. Today, aspirin remains the most commonly used medication for the treatment of pyrexia, pain, inflammation and antiplatelet. The present study aims at evaluating the possible existence of a putative p53-dependent pathway underlying the aspirin-induced inhibition of adipogenesis. Cell migration assay was identified by the ability to migrate through Transwell insert. Oil Red O staining was employed to quantify adipose accumulation. The concentration of glucose and triglyceride were measured by using assay kits. The expression levels of several master regulatory molecules controlling various signal pathways were monitored using the immunoblotting techniques. Aspirin significantly inhibited preadipocyte migration and adipose accumulation. The p53-p21 signaling and the expression of differentiation marker glycerol-3-phosphate dehydrogenase were increased in a dose-dependent manner. It indicated that aspirin induced adipocyte differentiation through p53-p21 pathway. The oncogenic ERK 1/2 MAPK signaling was induced, whereas, the expression of adipogenic markers peroxisome proliferator-activated receptor γ (PPARγ), adipocyte fatty acid-binding protein (A-FABP) and inflammatory factors cyclooxygenase-2 (Cox-2), tumor necrosis factor α (TNFα) and inducible nitric oxide synthase (iNOS) were inhibited. Aspirin negatively regulated the pentose phosphate pathway (PPP) by inhibiting the expression of rate-limiting enzyme glucose-6-phosphate dehydrogenase. Knockdown the expression of oncogenic ERK 1/2 MAPK by using 10 μM PD98059 significantly increased triglyceride synthesis, adipose accumulation and activated PPP, however, decreased glucose uptake. Diverted the glucose flux to PPP, rather than increased glucose uptake, was associated with adipogenesis. Down-regulated the expression of tumor suppressor p53 by 10 μM pifithrin-α (PFTα) alone had no effect on adipose accumulation. However, administration of aspirin accompanied with PFTα abolished aspirin-induced inhibition of adipogenesis. We demonstrated that aspirin-induced inhibition of adipogenesis was p53-dependent and associated with inactivation of PPP. Blockade PPP may be a novel strategy for obesity prevention and therapy. Moreover, when use aspirin in therapeutic strategy, the p53 status should be considered.