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Vitamin D Promotes Odontogenic Differentiation of Human Dental Pulp Cells via ERK Activation

  • Woo, Su-Mi (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Lim, Hae-Soon (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Jeong, Kyung-Yi (Department of Dental Hygiene, Honam University) ;
  • Kim, Seon-Mi (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Kim, Won-Jae (Dental Science Research Institute, School of Dentistry, Chonnam National University) ;
  • Jung, Ji-Yeon (Dental Science Research Institute, School of Dentistry, Chonnam National University)
  • Received : 2014.11.18
  • Accepted : 2015.04.28
  • Published : 2015.07.31

Abstract

The active metabolite of vitamin D such as $1{\alpha}$,25-dihydroxyvitamin ($D_3(1{\alpha},25(OH)_2D_3)$ is a well-known key regulatory factor in bone metabolism. However, little is known about the potential of vitamin D as an odontogenic inducer in human dental pulp cells (HDPCs) in vitro. The purpose of this study was to evaluate the effect of vitamin $D_3$ metabolite, $1{\alpha},25(OH)_2D_3$, on odontoblastic differentiation in HDPCs. HDPCs extracted from maxillary supernumerary incisors and third molars were directly cultured with $1{\alpha},25(OH)_2D_3$ in the absence of differentiation-inducing factors. Treatment of HDPCs with $1{\alpha},25(OH)_2D_3$ at a concentration of 10 nM or 100 nM significantly upregulated the expression of dentin sialophosphoprotein (DSPP) and dentin matrix protein1 (DMP1), the odontogenesis-related genes. Also, $1{\alpha},25(OH)_2D_3$ enhanced the alkaline phosphatase (ALP) activity and mineralization in HDPCs. In addition, $1{\alpha},25(OH)_2D_3$ induced activation of extracellular signal-regulated kinases (ERKs), whereas the ERK inhibitor U0126 ameliorated the upregulation of DSPP and DMP1 and reduced the mineralization enhanced by $1{\alpha},25(OH)_2D_3$. These results demonstrated that $1{\alpha},25(OH)_2D_3$ promoted odontoblastic differentiation of HDPCs via modulating ERK activation.

Keywords

References

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