• Journal of dental hygiene science
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• v.19 no.1
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• pp.39-47
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• 2019

Background: Light-emitting diodes curing unit (LCU), which emit blue light, is used for polymerization of composite resins in many dentistry. Although the use of LCU for light-cured composite resin polymerization is considered safe, it is still controversial whether it can directly or indirectly have harmful biological influences on oral tissues. The aim of this study was to elucidate the biological effects of LCU in wavelengths ranging from 440 to 490 nm, on the cell viability and secretion of inflammatory cytokines in MDPC-23 odontoblastic cells and inflammatory-induced MDPC-23 cells by lipopolysaccharide (LPS). Methods: The MTT assay and observation using microscope were performed on MDPC-23 cells to investigate the cell viability and cytotoxic effects on LCU irradiation. Results: MDPC-23 cells and LPS stimulated MDPC-23 cells were found to have no effects on cell viability and cell morphology in the LCU irradiation. Nitric oxide (NO) and prostaglandin $E_2$ which are the pro-inflammatory mediators, and interleukin-$1{\beta}$ and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) which are the proinflammatory cytokines were significantly increased in MCPD-23 cells after LCU irradiation as time increased in comparison with the control. LCU irradiation has the potential to induce inflammation or biological damages in normal dental tissues, including MDPC-23 cells. Conclusion: Therefore, it is necessary to limit the use of LCU except for the appropriate dose and irradiation time. In addition, LCU irradiation of inflammatory-induced MDPC-23 cells by LPS was reduced the secretion of NO compared to the LPS alone treatment group and was significantly reduced the secretion of TNF-${\alpha}$ in all the time groups. Therefore, LCU application in LPS stimulated MDPC-23 odontoblastic cells has a photodynamic therapy like effect as well as inflammation relief.

• Journal of the korean academy of Pediatric Dentistry
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• v.37 no.3
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• pp.308-316
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• 2010

Odontoblasts are anchorage dependent cells adhering to a substrate via cell adhesive molecules. Receptor ligands such as integrins bind to these proteins and are known to function as signal transduction molecules in a series of critical recognition events of cell-substratum. The aim of this study is to examine the interaction of odontoblast (MDPC-23 cell) with type I Col and the effect of TGF-${\beta}1$ and TNF-$\alpha$ on the expression of cell adhesion molecules. In this study, MDPC-23 cells adhered to type I Col dose-dependently. Immunofluorescence data demonstrated that integrin ${\alpha}1$, ${\alpha}2$ and CD44 were expressed on cell surface, and FAK and paxillin were localized in focal adhesion plaques in MDPC-23 cells adhesion to Col. Cytokine TGF-${\beta}1$ increased the adhesion of MDPC-23 cells to Col and the expression level of integrin ${\alpha}1$, 4{\alpha}2$ and chondroitin sulfate on MDPC-23 cells. RT-PCR data demonstrated that cytokine TGF-${\beta}1$ increased the amount of integrin ${\alpha}1$ mRNA in MDPC-23 cells. Therefore, MDPC-23 cells adhere to collagen type I Col and expressed a complex pattern of integrins and proteoglycans, including ${\alpha}1$, ${\alpha}2$, chondroitin sulfate and CD44 detected by immunoblotting and immunofluorescence assay. TGF-${\beta}1$ treatment enhanced the expression of adhesion molecules such as integrin ${\alpha}1$, ${\alpha}2$ and chondroitin sulfate.

• International Journal of Oral Biology
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• v.43 no.3
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• pp.133-140
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• 2018

Resveratrol (3,4',5,-trihydroxystilbene), a phytoalexin present in grapes, exerts a variety of actions to reduce superoxides, prevents diabetes mellitus, and inhibits inflammation. Resveratrol acts as a chemo-preventive agent and induces apoptotic cell death in various cancer cells. However, the role of resveratrol in odontoblastic cell differentiation is unclear. In this study, the effect of resveratrol on regulating odontoblast differentiation was examined in MDPC-23 mouse odontoblastic cells derived from mouse dental papilla cells. Resveratrol significantly accelerated mineralization as compared with the control culture in differentiation of MDPC-23 cells. Resveratrol significantly increased expression of ALP mRNA as compared with the control in differentiation of MDPC-23 cells. Resveratrol significantly accelerated expression of Col I mRNA as compared with the control in differentiation of MDPC-23 cells. Resveratrol significantly increased expressions of DSPP and DMP-1 mRNAs as compared with the control in differentiation of MDPC-23 cells. Treatment of resveratrol did not significantly affect cell proliferation in MDPC-23 cells. Results suggest resveratrol facilitates odontoblast differentiation and mineralization in differentiation of MDPC-23 cells, and may have potential properties for development and clinical application of dentin regeneration materials.

• International Journal of Oral Biology
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• v.37 no.3
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• pp.146-152
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• 2012

MicroRNAs (miRNAs, miRs) are about 21-25 nucleotides in length and regulate mRNA translation by base pairing to partially complementary sites, predominantly in the 3'-untranslated region (3'-UTR) of the target mRNA. In this study, the expression profile of miRNAs was compared and analyzed for the establishment of miRNA-related odontoblast differentiation using MDPC-23 cells derived from mouse dental papilla cells. To determine the expression profile of miRNAs during the differentiation of MDPC-23 cells, we employed miRNA microarray analysis, quantitative real-time PCR (qRT-PCR) and Alizaline red-S staining. In the miRNA microarray analysis, 11 miRNAs were found to be up- or down-regulated more than 3-fold between day 0 (control) and day 5 of MDPC-23 cell differentiation among the 1,769 miRNAs examined. In qRT-PCR analysis, the expression levels of two of these molecules, miR-194 and miR-126, were increased and decreased in the control MDPC-23 cells compared with the MDPC-23 cells at day 5 of differentiation, respectively. Importantly, the overexpression of miR-194 significantly accelerated mineralization compared with the control cultures during the differentiation of MDPC-23 cells. These results suggest that the miR-194 augments MDPC-23 cell differentiation, and potently accelerates the mineralization process. Moreover, these in vitro results show that different miRNAs are deregulated during the differentiation of MDPC-23 cells, suggesting the involvement of these genes in the differentiation and mineralization of odontoblasts.

• Journal of Korean society of Dental Hygiene
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• v.17 no.3
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• pp.441-448
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• 2017

Objectives: The purpose of this study was to examine the cell proliferation and expression of alkaline phosphatase (ALP) during the differentiation of murine odontoblast-like cells (MDPC-23) by Cimicifuga rhizoma extract. Cimicifuga rhizoma extract was prepared using 70% ethanol. Then, the cells were treated with 25, 50, 100, 150, and $200{\mu}g$ of Cimicifuga rhizoma extract. Methods: We determined the Cimicifuga rhizoma effects of MDPC-23 using WST-1 (water soluble tetrazolium salt-1) assay, ALP activity assay and histochemical staining. Results: $25-200{\mu}g$ of Cimicifuga rhizoma extract did not inhibit the growth of MDPC-23 cells; $100{\pm}0$, $100{\pm}3.29$, $99{\pm}4.86$, $98{\pm}3.80$, $98{\pm}1.73$, $99{\pm}5.05%$ (p<0.794). $50{\mu}g$ of Cimicifuga rhizoma extract stimulated ALP activity on MDPC-23; $5.1{\pm}0.20units/{\mu}{\ell}$ (p<0.001). Conclusions: It was proven that Cimicifuga rhizoma promoted differentiation of MDPC- 23 cells.

• International Journal of Oral Biology
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• v.33 no.4
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• pp.187-195
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• 2008

Reparative dentine formation requires newly differentiated odontoblast-like cells. Therefore, identification of the molecule that stimulates the odontogenic differentiation of precursor cells in the tooth pulp will be helpful for the development of strategies to repair damaged pulp. In this study, we examined the effect of N-acetylcysteine (NAC) on the odontogenic differentiation of MDPC-23 cells, a mouse odontoblast-like cell line derived from dental papilla, and primary cultured rat dental papilla cells (RDPCs). NAC (1-30 mM) suppressed production of reactive oxygen species in MDPC-23 cells in a dose-dependent manner. Although 5 to 20 mM NAC did not alter MDPC-23 cell proliferation, 1 or 30 mM NAC significantly inhibited it. NAC enhanced mineralized nodule formation and the expression of several odontoblast differentiation-associated genes in both RDPCs and MDPC-23. This NAC stimulatory effect was significant, even at concentrations lower than 1 mM. However, NAC did not stimulate expression of bone morphogenetic protein-2, -4, or -7, which are known to enhance odontogenic differentiation. Since reactive oxygen species are also involved in the pulp toxicity of resin-based restorative materials, these results suggest that NAC may be a promising candidate for supplementation of dental restorative materials in order to enhance reparative dentine formation.

• International Journal of Oral Biology
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• v.42 no.2
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• pp.39-45
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• 2017

Metformin (1,1-dimethylbiguanide hydrochloride), derived from French lilac (Galega officinalis), is a first-line anti-diabetic drug prescribed for patients with type 2 diabetes. However, the role of metformin in odontoblastic cell differentiation is still unclear. This study therefore undertook to examine the effect of metformin on regulating odontoblast differentiation in MDPC-23 mouse odontoblastic cells derived from mouse dental papilla cells. As compared to controls, metformin significantly accelerated the mineralization, significantly increased and accelerated the expressions of ALP and Col I mRNAs, and significantly increased the accelerated expressions of DSPP and DMP-1 mRNAs, during differentiation of MDPC-23 cells. There was no alteration in cell proliferation of MDPC-23 cells, on exposure to metformin. These results suggest that the effect of metformin on MDPC-23 mouse odontoblastic cells derived from mouse dental papilla cells, facilitates the odontoblast differentiation and mineralization, without altering the cell proliferation.

• Journal of Korean society of Dental Hygiene
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• v.14 no.5
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• pp.775-781
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• 2014

Objectives : The purpose of the study is to investigate the protective effect of coenzyme $Q_{10}$ on cytotoxicity effect of dental monomers in odontoblast(MDPC-23). Methods : MDPC-23 was incubated with the(co)monomers triethylene glycol dimethacrylate (TEGDMA) with and without addition of coenzyme $Q_{10}$. The cell proliferation and survival was determined using WST-1 assay. The level of reactive oxygen species(ROS) was measured by immunofluorescent staining for DCF-DA. Results : TEGDMA treatment decreased the cell proliferation by dose dependently(0.1, 1, 2.5, 5, 10 mM) on the growth of MDPC-23 cells. Coenzyme $Q_{10}$ showed cell proliferation from 5 to $500{\mu}M$ by WST-1 assay. Pre-treatment coenzyme $Q_{10}$ showed the antioxidant effect on proliferation and viability of MDPC-23 after 48h(p<0.05). The positive cells were observed in non-coenyme $Q_{10}$ treatment group(group 2) in comparison with coenyme $Q_{10}$ pre-treatment group(group 1) by DCF-DA. The fluorescence positive cells showed 14.715(group 1) and 19.788(group 2) using image J system. Conclusions : TEGDMA induced cytotoxicity. The MDPC-23 cell death was associated with the increasing ROS. Coenyme $Q_{10}$ showed the antioxidant effects by decreasing ROS. This effects may contribute to the treatment of periodontal disease induced by TEGDMA after operation.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.1
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• pp.37-45
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• 2022

The aim of the present study was to investigate the physiological role of nicotinamide phosphoribosyltransferase (NAMPT) associated with odontogenic differentiation during tooth development in mice. Mouse dental papilla cell-23 (MDPC-23) cells cultured in differentiation media were stimulated with the specific NAMPT inhibitor, FK866, and Visfatin (NAMPT) for up to 10 days. The cells were evaluated after 0, 4, 7, and 10 days. Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The mineralization assay was performed by staining MDPC-23 cells with Alizarin Red S solution. After cultivation, MDPC-23 cells were harvested for quantitative PCR or Western blotting. Analysis of variance was performed using StatView 5.0 software (SAS Institute Inc., Cary, NC, USA). Statistical significance was set at p < 0.05. The expression of NAMPT increased during the differentiation of murine odontoblast-like MDPC-23 cells. Furthermore, the up-regulation of NAMPT promoted odontogenic differentiation and accelerated mineralization through an increase in representative odontoblastic biomarkers, such as dentin sialophosphoprotein, dentin matrix protein-1, and alkaline phosphatase in MDPC-23 cells. However, treatment of the cells with the NAMPT inhibitor, FK866, attenuated odontogenic differentiation, as evidenced by the suppression of odontoblastic biomarkers. These data indicate that NAMPT regulated odontoblastic differentiation through the regulation of odontoblastic biomarkers. The increase in NAMPT expression in odontoblasts was closely related to the formation of the extracellular matrix and dentin via the Runx signaling pathway. Therefore, these data suggest that NAMPT is a critical regulator of odontoblast differentiation during tooth development.

• International Journal of Oral Biology
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• v.40 no.4
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• pp.197-204
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• 2015

MicroRNA (miRNA, miR) is essential in regulating cell differentiation either by inhibiting mRNA translation or by inducing its degradation. However, the role of miRNA in odontoblastic cell differentiation is still unclear. In this study, we examined the molecular mechanism of miR-27-mediated regulation of odontoblast differentiation in MDPC-23 mouse odontoblastic cells derived from mouse dental papilla cells. The results of the present study demonstrated that the miR-27 expression increases significantly during MDPC-23 odontoblastic cell differentiation. Furthermore, miR-27 up-regulation promotes the differentiation of MDPC-23 cells and accelerates mineralization without cell proliferation. The over-expression of miR-27 significantly increased the expression levels of Wnt1 mRNA and protein. In addition, the results of target gene prediction revealed that Wnt1 mRNA has an miR-27 binding site in its 3'UTR, and is increased by miR-27. These results suggested that miR-27 promotes MDPC-23 odontoblastic cell differentiation by targeting Wnt1 signaling. Therefore, miR-27 is a critical odontoblastic differentiation molecular target for the development of miRNA based therapeutic agents in dental medicine.