Nicotinamide phosphoribosyltransferase regulates the cell differentiation and mineralization in cultured odontoblasts
Kyeong-Rok Kang1, Jae-Sung Kim1, Jeong-Yeon Seo1,2, HyangI Lim1, Tae-Hyeon Kim1, Sun-Kyoung Yu1, Heung-Joong Kim1, Chun Sung Kim1, Hong Sung Chun2, Joo-Cheol Park3, and Do Kyung Kim1,*
1The Institute of Dental Science, Chosun University, 2Department of Integrative Biological Sciences & BK21 FOUR Educational Research Group for Ageassociated Disorder Control Technology, Chosun University, Gwangju 61452, 3Laboratory for the Study of Regenerative Dental Medicine, Department of Oral Histology-Developmental Biology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul 08826, Korea
Received: October 13, 2021; Revised: November 16, 2021; Accepted: November 23, 2021
This is an Open Access journal distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Keywords: Differentiation, Nicotinamide phosphoribosyltransferase, Odontoblasts, Tooth development